Journal articles
Astara K, Pournara C, de Natale ER, Wilson H, Vavougios GD, Lappas AS, Politis M, Christodoulou NG (2023). A novel conceptual framework for the functionality of the glymphatic system.
J Neurophysiol,
129(5), 1228-1236.
Abstract:
A novel conceptual framework for the functionality of the glymphatic system.
The glymphatic system is responsible for the clearance of the potentially harmful metabolic waste of the central nervous system. The prevalent theory is that the cerebrospinal fluid (CSF) circulates in the perivascular space (PVS) and through the astrocytes' aquaporin-4 channels (AQ-4), and it is then drained by the lymphatic vessels after mixing with interstitial fluid (ISF). However, there is little evidence supporting this hypothesis. A deeper understanding of the physiology of the glymphatic system could transform the way we understand neuropathology and our approach to treating neurological and neuropsychiatric disorders. In this review, we introduce a new conceptual framework for the functionality of the glymphatic system, offering new directions for future research. We propose that CSF and ISF exchange flow depends on arterial pulsation, respiration, posture, and sleep. PVS changes due to disrupted cerebral autoregulation, alternations of intrathoracic pressure, venous flow, and body position can also influence the glymphatic flow. The role of respiration remains controversial due to the variety of parameters that interfere with glymphatic functionality. Slow-wave sleep is important for glymphatic clearance due to neuronal electromagnetic synchronization and expansion of the interstitial space. Therefore, sleep and vascular disorders, as well as aging, may hinder glymphatic flow and induce a noxious milieu of susceptibility to neurodegenerative disorders because of metabolic waste accumulation. We lastly introduce a new idea postulating that electromagnetic induction may constitute one of the propelling forces for the convectional current and mixing of CSF and ISF.
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Qamar MA, Sauerbier A, Politis M, Carr H, Loehrer PA, Chaudhuri KR (2023). Author Correction: Presynaptic dopaminergic terminal imaging and non-motor symptoms assessment of Parkinson’s disease: evidence for dopaminergic basis? (npj Parkinson's Disease, (2017), 3, 1, (5), 10.1038/s41531-016-0006-9).
npj Parkinson's Disease,
9(1).
Abstract:
Author Correction: Presynaptic dopaminergic terminal imaging and non-motor symptoms assessment of Parkinson’s disease: evidence for dopaminergic basis? (npj Parkinson's Disease, (2017), 3, 1, (5), 10.1038/s41531-016-0006-9)
In this article the author name PA Loehrer was incorrectly written as P Loehrer. The original article has been corrected.
Abstract.
Erritzoe D, Godlewska BR, Rizzo G, Searle GE, Agnorelli C, Lewis Y, Ashok AH, Colasanti A, Boura I, Farrell C, et al (2023). Brain Serotonin Release is Reduced in Patients with Depression: a [<sup>11</sup>C]Cimbi-36 Positron Emission Tomography Study with a d-Amphetamine Challenge.
Biological Psychiatry,
93(12), 1089-1098.
Abstract:
Brain Serotonin Release is Reduced in Patients with Depression: a [11C]Cimbi-36 Positron Emission Tomography Study with a d-Amphetamine Challenge
Background: the serotonin hypothesis of depression proposes that diminished serotonergic (5-HT) neurotransmission is causal in the pathophysiology of the disorder. Although the hypothesis is over 50 years old, there is no firm in vivo evidence for diminished 5-HT neurotransmission. We recently demonstrated that the 5-HT2A receptor agonist positron emission tomography (PET) radioligand [11C]Cimbi-36 is sensitive to increases in extracellular 5-HT induced by an acute d-amphetamine challenge. Here we applied [11C]Cimbi-36 PET to compare brain 5-HT release capacity in patients experiencing a major depressive episode (MDE) to that of healthy control subjects (HCs) without depression. Methods: Seventeen antidepressant-free patients with MDE (3 female/14 male, mean age 44 ± 13 years, Hamilton Depression Rating Scale score 21 ± 4 [range 16–30]) and 20 HCs (3 female/17 male, mean age 32 ± 9 years) underwent 90-minute dynamic [11C]Cimbi-36 PET before and 3 hours after a 0.5-mg/kg oral dose of d-amphetamine. Frontal cortex (main region of interest) 5-HT2A receptor nondisplaceable binding was calculated from kinetic analysis using the multilinear analysis-1 approach with the cerebellum as the reference region. Results: Following d-amphetamine administration, frontal nondisplaceable binding potential (BPND) was significantly reduced in the HC group (1.04 ± 0.31 vs. 0.87 ± 0.24, p <. 001) but not in the MDE group (0.97 ± 0.25 vs. 0.92 ± 0.22, not significant). ΔBPND of the MDE group was significantly lower than that of the HC group (HC: 15% ± 14% vs. MDE: 6.5% ± 20%, p =. 041). Conclusions: This first direct assessment of 5-HT release capacity in people with depression provides clear evidence for dysfunctional serotonergic neurotransmission in depression by demonstrating reduced 5-HT release capacity in patients experiencing an MDE.
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Ford J, Kafetsouli D, Wilson H, Udeh-Momoh C, Politis M, AhmadiAbhari S, Rabiner I, Middleton LT (2022). At a Glance: an Update on Neuroimaging and Retinal Imaging in Alzheimer's Disease and Related Research.
J Prev Alzheimers Dis,
9(1), 67-76.
Abstract:
At a Glance: an Update on Neuroimaging and Retinal Imaging in Alzheimer's Disease and Related Research.
Neuroimaging serves a variety of purposes in Alzheimer's disease (AD) and related dementias (ADRD) research - from measuring microscale neural activity at the subcellular level, to broad topological patterns seen across macroscale-brain networks, and everything in between. In vivo imaging provides insight into the brain's structure, function, and molecular architecture across numerous scales of resolution; allowing examination of the morphological, functional, and pathological changes that occurs in patients across different AD stages (1). AD is a complex and potentially heterogenous disease, with no proven cure and no single risk factor to isolate and measure, whilst known risk factors do not fully account for the risk of developing this disease (2). Since the 1990's, technological advancements in neuroimaging have allowed us to visualise the wide organisational structure of the brain (3) and later developments led to capturing information of brain 'functionality', as well as the visualisation and measurement of the aggregation and accumulation of AD-related pathology. Thus, in vivo brain imaging has and will continue to be an instrumental tool in clinical research, mainly in the pre-clinical disease stages, aimed at elucidating the biological complex processes and interactions underpinning the onset and progression of cognitive decline and dementia. The growing societal burden of AD/ADRD means that there has never been a greater need, nor a better time, to use such powerful and sensitive tools to aid our understanding of this undoubtedly complex disease. It is by consolidating and reflecting on these imaging advancements and developing long-term strategies across different disciplines, that we can move closer to our goal of dementia prevention. This short commentary will outline recent developments in neuroimaging in the field of AD and dementia by first describing the historical context of AD classification and the introduction of AD imaging biomarkers, followed by some examples of significant recent developments in neuroimaging methods and technologies.
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Wilson H, Pagano G, Yousaf T, Polychronis S, De Micco R, Giordano B, Niccolini F, Politis M (2022). Correction to: Predict cognitive decline with clinical markers in Parkinson's disease (PRECODE-1).
J Neural Transm (Vienna),
129(10).
Author URL.
Siderowf A, Seibyl J, Coffey C, Tosun-Turgut D, Shaw LM, Trojanowski JQ, Singleton A, Kieburtz K, Toga A, Mollenhauer B, et al (2022). Longitudinal clinical and biomarker characteristics of non-manifesting LRRK2 G2019S carriers in the PPMI cohort. npj Parkinson's Disease, 8(1).
de Natale ER, Wilson H, Politis M (2022). Predictors of RBD progression and conversion to synucleinopathies.
Curr Neurol Neurosci Rep,
22(2), 93-104.
Abstract:
Predictors of RBD progression and conversion to synucleinopathies.
PURPOSE OF REVIEW: Rapid eye movement (REM) sleep behaviour disorder (RBD) is considered the expression of the initial neurodegenerative process underlying synucleinopathies and constitutes the most important marker of their prodromal phase. This article reviews recent research from longitudinal research studies in isolated RBD (iRBD) aiming to describe the most promising progression biomarkers of iRBD and to delineate the current knowledge on the level of prediction of future outcome in iRBD patients at diagnosis. RECENT FINDINGS: Longitudinal studies revealed the potential value of a variety of biomarkers, including clinical markers of motor, autonomic, cognitive, and olfactory symptoms, neurophysiological markers such as REM sleep without atonia and electroencephalography, genetic and epigenetic markers, cerebrospinal fluid and serum markers, and neuroimaging markers to track the progression and predict phenoconversion. To-date the most promising neuroimaging biomarker in iRBD to aid the prediction of phenoconversion is striatal presynaptic striatal dopaminergic dysfunction. There is a variety of potential biomarkers for monitoring disease progression and predicting iRBD conversion into synucleinopathies. A combined multimodal biomarker model could offer a more sensitive and specific tool. Further longitudinal studies are warranted to iRBD as a high-risk population for early neuroprotective interventions and disease-modifying therapies.
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Wilson H, de Natale ER, Politis M (2022). Recent Advances in Neuroimaging Techniques to Assist Clinical Trials on Cell-Based Therapies in Neurodegenerative Diseases.
Stem Cells,
40(8), 724-735.
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Recent Advances in Neuroimaging Techniques to Assist Clinical Trials on Cell-Based Therapies in Neurodegenerative Diseases.
Neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD), are progressive disorders for which curative therapy is still lacking. Cell-based therapy aims at replacing dysfunctional cellular populations by repairing damaged tissue and by enriching the microenvironment of selective brain areas, and thus constitutes a promising disease-modifying treatment of neurodegenerative diseases. Scientific research has engineered a wide range of human-derived cellular populations to help overcome some of the logistical, safety, and ethical issues associated with this approach. Open-label studies and clinical trials in human participants have used neuroimaging techniques, such as positron emission tomography (PET) and magnetic resonance imaging (MRI), to assess the success of the transplantation, to evaluate the functional integration of the implanted tissue into the host environment and to understand the pathophysiological changes associated with the therapy. Neuroimaging has constituted an outcome measure of large, randomized clinical trials, and has given answers to clarify the pathophysiology underlying some of the complications linked with this therapy. Novel PET radiotracers and MRI sequences for the staging of neurodegenerative diseases and to study alterations at the molecular level significantly expands the translational potential of neuroimaging to assist pre-clinical and clinical research on cell-based therapy in these disorders. This concise review summarizes the current use of neuroimaging in human studies of cell-based replacement therapy and focuses on the future applications of PET and MRI techniques to evaluate the pathophysiology and treatment efficacy, as well as to aid patient selection and as an outcome measure to improve treatment success.
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Verghese JP, Terry A, de Natale ER, Politis M (2022). Research Evidence of the Role of the Glymphatic System and its Potential Pharmacological Modulation in Neurodegenerative Diseases.
J Clin Med,
11(23).
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Research Evidence of the Role of the Glymphatic System and its Potential Pharmacological Modulation in Neurodegenerative Diseases.
The glymphatic system is a unique pathway that utilises end-feet Aquaporin 4 (AQP4) channels within perivascular astrocytes, which is believed to cause cerebrospinal fluid (CSF) inflow into perivascular space (PVS), providing nutrients and waste disposal of the brain parenchyma. It is theorised that the bulk flow of CSF within the PVS removes waste products, soluble proteins, and products of metabolic activity, such as amyloid-β (Aβ). In the experimental model, the glymphatic system is selectively active during slow-wave sleep, and its activity is affected by both sleep dysfunction and deprivation. Dysfunction of the glymphatic system has been proposed as a potential key driver of neurodegeneration. This hypothesis is indirectly supported by the close relationship between neurodegenerative diseases and sleep alterations, frequently occurring years before the clinical diagnosis. Therefore, a detailed characterisation of the function of the glymphatic system in human physiology and disease would shed light on its early stage pathophysiology. The study of the glymphatic system is also critical to identifying means for its pharmacological modulation, which may have the potential for disease modification. This review will critically outline the primary evidence from literature about the dysfunction of the glymphatic system in neurodegeneration and discuss the rationale and current knowledge about pharmacological modulation of the glymphatic system in the animal model and its potential clinical applications in human clinical trials.
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Chandra A, Farrell C, Wilson H, Dervenoulas G, De Natale ER, Politis M (2021). Aquaporin-4 polymorphisms predict amyloid burden and clinical outcome in the Alzheimer's disease spectrum. Neurobiology of Aging, 97, 1-9.
King-Robson J, Wilson H, Politis M, Alzheimer’s Disease Neuroimaging Initiative (2021). Associations Between Amyloid and Tau Pathology, and Connectome Alterations, in Alzheimer's Disease and Mild Cognitive Impairment.
J Alzheimers Dis,
82(2), 541-560.
Abstract:
Associations Between Amyloid and Tau Pathology, and Connectome Alterations, in Alzheimer's Disease and Mild Cognitive Impairment.
BACKGROUND: the roles of amyloid-β and tau in the degenerative process of Alzheimer's disease (AD) remain uncertain. [18F]AV-45 and [18F]AV-1451 PET quantify amyloid-β and tau pathology, respectively, while diffusion tractography enables detection of their microstructural consequences. OBJECTIVE: Examine the impact of amyloid-β and tau pathology on the structural connectome and cognition, in mild cognitive impairment (MCI) and AD. METHODS: Combined [18F]AV-45 and [18F]AV-1451 PET, diffusion tractography, and cognitive assessment in 28 controls, 32 MCI, and 26 AD patients. RESULTS: Hippocampal connectivity was reduced to the thalami, right lateral orbitofrontal, and right amygdala in MCI; alongside the insula, posterior cingulate, right entorhinal, and numerous cortical regions in AD (all p
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Politis M (2021). Erratum to “The role of phosphodiesterase 4 in excessive daytime sleepiness in Parkinson's disease” [Park. Relat. Disord. 77C (2021) 163–169/3948] (Parkinsonism and Related Disorders (2020) 77 (163–169), (S1353802019300732), (10.1016/j.parkreldis.2019.02.027)).
Parkinsonism and Related Disorders,
88, 58-59.
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Erratum to “The role of phosphodiesterase 4 in excessive daytime sleepiness in Parkinson's disease” [Park. Relat. Disord. 77C (2021) 163–169/3948] (Parkinsonism and Related Disorders (2020) 77 (163–169), (S1353802019300732), (10.1016/j.parkreldis.2019.02.027))
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Simuni T, Uribe L, Cho HR, Caspell-Garcia C, Coffey CS, Siderowf A, Trojanowski JQ, Shaw LM, Seibyl J, Singleton A, et al (2020). Clinical and dopamine transporter imaging characteristics of non-manifest LRRK2 and GBA mutation carriers in the Parkinson's Progression Markers Initiative (PPMI): a cross-sectional study.
The Lancet Neurology,
19(1), 71-80.
Abstract:
Clinical and dopamine transporter imaging characteristics of non-manifest LRRK2 and GBA mutation carriers in the Parkinson's Progression Markers Initiative (PPMI): a cross-sectional study
Background: the Parkinson's Progression Markers Initiative (PPMI) is an ongoing observational, longitudinal cohort study of participants with Parkinson's disease, healthy controls, and carriers of the most common Parkinson's disease-related genetic mutations, which aims to define biomarkers of Parkinson's disease diagnosis and progression. All participants are assessed annually with a battery of motor and non-motor scales, 123-I Ioflupane dopamine transporter (DAT) imaging, and biological variables. We aimed to examine whether non-manifesting carriers of LRRK2 and GBA mutations have prodromal features of Parkinson's disease that correlate with reduced DAT binding. Methods: This cross-sectional analysis is based on assessments done at enrolment in the subset of non-manifesting carriers of LRRK2 and GBA mutations enrolled into the PPMI study from 33 participating sites worldwide. The primary objective was to examine baseline clinical and DAT imaging characteristics in non-manifesting carriers with GBA and LRRK2 mutations compared with healthy controls. DAT deficit was defined as less than 65% of putamen striatal binding ratio expected for the individual's age. We used t tests, χ2 tests, and Fisher's exact tests to compare baseline demographics across groups. An inverse probability weighting method was applied to control for potential confounders such as age and sex. To account for multiple comparisons, we applied a family-wise error rate to each set of analyses. This study is registered with ClinicalTrials.gov, number NCT01141023. Findings: Between Jan 1, 2014, and Jan 1, 2019, the study enrolled 208 LRRK2 (93% G2019S) and 184 GBA (96% N370S) non-manifesting carriers. Both groups were similar with respect to mean age, and about 60% were female. of the 286 (73%) non-manifesting carriers that had DAT imaging results, 18 (11%) LRRK2 and four (3%) GBA non-manifesting carriers had a DAT deficit. Compared with healthy controls, both LRRK2 and GBA non-manifesting carriers had significantly increased mean scores on the Movement Disorders Society Unified Parkinson's Disease Rating Scale (total score 4·6 [SD 4·4] healthy controls vs 8·4 [7·3] LRRK2 vs 9·5 [9·2] GBA, p
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Carotenuto A, Wilson H, Giordano B, Caminiti SP, Chappell Z, Williams SCR, Hammers A, Silber E, Brex P, Politis M, et al (2020). Impaired connectivity within neuromodulatory networks in multiple sclerosis and clinical implications.
Journal of Neurology,
267(7), 2042-2053.
Abstract:
Impaired connectivity within neuromodulatory networks in multiple sclerosis and clinical implications
AbstractThere is mounting evidence regarding the role of impairment in neuromodulatory networks for neurodegenerative diseases, such as Parkinson’s and Alzheimer’s disease. However, the role of neuromodulatory networks in multiple sclerosis (MS) has not been assessed. We applied resting-state functional connectivity and graph theory to investigate the changes in the functional connectivity within neuromodulatory networks including the serotonergic, noradrenergic, cholinergic, and dopaminergic systems in MS. Twenty-nine MS patients and twenty-four age- and gender-matched healthy controls performed clinical and cognitive assessments including the expanded disability status score, symbol digit modalities test, and Hamilton Depression rating scale. We demonstrated a diffuse reorganization of network topography (P < 0.01) in serotonergic, cholinergic, noradrenergic, and dopaminergic networks in patients with MS. Serotonergic, noradrenergic, and cholinergic network functional connectivity derangement was associated with disease duration, EDSS, and depressive symptoms (P < 0.01). Derangements in serotonergic, noradrenergic, cholinergic, and dopaminergic network impairment were associated with cognitive abilities (P < 0.01). Our results indicate that functional connectivity changes within neuromodulatory networks might be a useful tool in predicting disability burden over time, and could serve as a surrogate endpoint to assess efficacy for symptomatic treatments.
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Wilson H, Pagano G, de Natale ER, Mansur A, Caminiti SP, Polychronis S, Middleton LT, Price G, Schmidt KF, Gunn RN, et al (2020). Mitochondrial Complex 1, Sigma 1, and Synaptic Vesicle 2A in Early Drug-Naive Parkinson's Disease.
Mov Disord,
35(8), 1416-1427.
Abstract:
Mitochondrial Complex 1, Sigma 1, and Synaptic Vesicle 2A in Early Drug-Naive Parkinson's Disease.
BACKGROUND: Dysfunction of mitochondrial energy generation may contribute to neurodegeneration, leading to synaptic loss in Parkinson's disease (PD). The objective of this study was to find cross-sectional and longitudinal changes in PET markers of synaptic vesicle protein 2A, sigma 1 receptor, and mitochondrial complex 1 in drug-naive PD patients. METHODS: Twelve early drug-naive PD patients and 16 healthy controls underwent a 3-Tesla MRI and PET imaging to quantify volume of distribution of [11 C]UCB-J, [11 C]SA-4503, and [18 F]BCPP-EF for synaptic vesicle protein 2A, sigma 1 receptor, and mitochondrial complex 1, respectively. Nine PD patients completed approximately 1-year follow-up assessments. RESULTS: Reduced [11 C]UCB-J volume of distribution in the caudate, putamen, thalamus, brain stem, and dorsal raphe and across cortical regions was observed in drug-naive PD patients compared with healthy controls. [11 C]UCB-J volume of distribution was reduced in the locus coeruleus and substantia nigra but did not reach statistical significance. No significant differences were found in [11 C]SA-4503 and [18 F]BCPP-EF volume of distribution in PD compared with healthy controls. Lower brain stem [11 C]UCB-J volume of distribution correlated with Movement Disorder Society Unified Parkinson's Disease Rating Scale part III and total scores. No significant longitudinal changes were identified in PD patients at follow-up compared with baseline. CONCLUSIONS: Our findings represent the first in vivo evidence of mitochondrial, endoplasmic reticulum, and synaptic dysfunction in drug-naive PD patients. Synaptic dysfunction likely occurs early in disease pathophysiology and has relevance to symptomatology. Mitochondrial complex 1 and sigma 1 receptor pathology warrants further investigations in PD. Studies in larger cohorts with longer follow-up will determine the validity of these PET markers to track disease progression. © 2020 the Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
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Wilson H, Politis M, Rabiner EA, Middleton LT (2020). Novel PET Biomarkers to Disentangle Molecular Pathways across Age-Related Neurodegenerative Diseases.
Cells,
9(12), 2581-2581.
Abstract:
Novel PET Biomarkers to Disentangle Molecular Pathways across Age-Related Neurodegenerative Diseases
There is a need to disentangle the etiological puzzle of age-related neurodegenerative diseases, whose clinical phenotypes arise from known, and as yet unknown, pathways that can act distinctly or in concert. Enhanced sub-phenotyping and the identification of in vivo biomarker-driven signature profiles could improve the stratification of patients into clinical trials and, potentially, help to drive the treatment landscape towards the precision medicine paradigm. The rapidly growing field of neuroimaging offers valuable tools to investigate disease pathophysiology and molecular pathways in humans, with the potential to capture the whole disease course starting from preclinical stages. Positron emission tomography (PET) combines the advantages of a versatile imaging technique with the ability to quantify, to nanomolar sensitivity, molecular targets in vivo. This review will discuss current research and available imaging biomarkers evaluating dysregulation of the main molecular pathways across age-related neurodegenerative diseases. The molecular pathways focused on in this review involve mitochondrial dysfunction and energy dysregulation; neuroinflammation; protein misfolding; aggregation and the concepts of pathobiology, synaptic dysfunction, neurotransmitter dysregulation and dysfunction of the glymphatic system. The use of PET imaging to dissect these molecular pathways and the potential to aid sub-phenotyping will be discussed, with a focus on novel PET biomarkers.
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Wilson H, Pagano G, Niccolini F, Muhlert N, Mehta MA, Searle G, Gunn RN, Rabiner EA, Foltynie T, Politis M, et al (2020). The role of phosphodiesterase 4 in excessive daytime sleepiness in Parkinson's disease.
Parkinsonism and Related Disorders,
77, 163-169.
Abstract:
The role of phosphodiesterase 4 in excessive daytime sleepiness in Parkinson's disease
Introduction: Preclinical studies suggest a link between cAMP/PKA signalling, phosphodiesterase 4 (PDE4) expression and excessive daytime sleepiness (EDS). Here, we investigated in vivo the association between PDE4 expression and EDS in Parkinson's disease (PD) patients using [11C]rolipram PET and MR imaging. Methods: Eighteen participants, 12 PD and 6 healthy controls, underwent one [11C]rolipram PET and a multi-modal MRI scan. Probabilistic tractography was performed on subjects’ diffusion data to functionally parcellate the striatum according with projections to limbic cortical areas. The severity of EDS was assessed using the Epworth Sleepiness Scale (ESS). To assess PDE4 expression in PD patients with EDS, the PD cohort was divided according to the presence (n = 5) or absence (n = 7) of EDS, defined using validated cut-off of score ≥10 on the ESS as score ≥10 on the ESS. Results: PD patients with EDS showed significantly increased [11C]rolipram volume of distribution (VT) in the caudate (P = 0.029), hypothalamus (P = 0.013), hippocampus (P = 0.036) and limbic striatum (P = 0.030) compared to patients without EDS. Furthermore, higher ESS scores correlated with increased [11C]rolipram VT in the caudate (r = 0.77; P = 0.003), hypothalamus (r = 0.84; P = 0.001), hippocampus (r = 0.81; P = 0.001) and limbic subdivisions of the striatum (r = 0.80; P = 0.003). Conclusion: Our findings translate into humans preclinical data indicating that EDS is associated with elevated PDE4 in regions regulating sleep. The severity of EDS in PD was associated with elevated PDE4 expression; thus, suggesting a role of PDE4 in the pathophysiology of EDS in PD.
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Carotenuto A, Giordano B, Dervenoulas G, Wilson H, Veronese M, Chappell Z, Polychronis S, Pagano G, Mackewn J, Turkheimer FE, et al (2020). [18F]Florbetapir PET/MR imaging to assess demyelination in multiple sclerosis.
Eur J Nucl Med Mol Imaging,
47(2), 366-378.
Abstract:
[18F]Florbetapir PET/MR imaging to assess demyelination in multiple sclerosis.
PURPOSE: We evaluated myelin changes throughout the central nervous system in Multiple Sclerosis (MS) patients by using hybrid [18F]florbetapir PET-MR imaging. METHODS: We included 18 relapsing-remitting MS patients and 12 healthy controls. Each subject performed a hybrid [18F]florbetapir PET-MR and both a clinical and cognitive assessment. [18F]florbetapir binding was measured as distribution volume ratio (DVR), through the Logan graphical reference method and the supervised cluster analysis to extract a reference region, and standard uptake value (SUV) in the 70-90 min interval after injection. The two quantification approaches were compared. We also evaluated changes in the measures derived from diffusion tensor imaging and arterial spin labeling. RESULTS: [18F]florbetapir DVRs decreased from normal-appearing white matter to the centre of T2 lesion (P
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Chandra A, Valkimadi P-E, Pagano G, Cousins O, Dervenoulas G, Politis M, Alzheimer's Disease Neuroimaging Initiative (2019). Applications of amyloid, tau, and neuroinflammation PET imaging to Alzheimer's disease and mild cognitive impairment.
Hum Brain Mapp,
40(18), 5424-5442.
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Applications of amyloid, tau, and neuroinflammation PET imaging to Alzheimer's disease and mild cognitive impairment.
Alzheimer's disease (AD) is a devastating and progressive neurodegenerative disease for which there is no cure. Mild cognitive impairment (MCI) is considered a prodromal stage of the disease. Molecular imaging with positron emission tomography (PET) allows for the in vivo visualisation and tracking of pathophysiological changes in AD and MCI. PET is a very promising methodology for differential diagnosis and novel targets of PET imaging might also serve as biomarkers for disease-modifying therapeutic interventions. This review provides an overview of the current status and applications of in vivo molecular imaging of AD pathology, specifically amyloid, tau, and microglial activation. PET imaging studies were included and evaluated as potential biomarkers and for monitoring disease progression. Although the majority of radiotracers showed the ability to discriminate AD and MCI patients from healthy controls, they had various limitations that prevent the recommendation of a single technique or tracer as an optimal biomarker. Newer research examining amyloid, tau, and microglial PET imaging in combination suggest an alternative approach in studying the disease process.
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Norgaard M, Ganz M, Svarer C, Feng L, Ichise M, Lanzenberger R, Lubberink M, Parsey RV, Politis M, Rabiner EA, et al (2019). Cerebral serotonin transporter measurements with [<SUP>11</SUP>C]DASB: a review on acquisition and preprocessing across 21 PET centres.
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM,
39(2), 210-222.
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Pagano G, Niccolini F, Wilson H, Yousaf T, Khan NL, Martino D, Plisson C, Gunn RN, Rabiner EA, Piccini P, et al (2019). Comparison of phosphodiesterase 10A and dopamine transporter levels as markers of disease burden in early Parkinson's disease.
Movement Disorders,
34(10), 1505-1515.
Abstract:
Comparison of phosphodiesterase 10A and dopamine transporter levels as markers of disease burden in early Parkinson's disease
Background: Recent work has shown loss of phosphodiesterase 10A levels in middle-stage and advanced treated patients with PD, which was associated with motor symptom severity. Objectives: to assess phosphodiesterase 10A levels in early PD and compare with loss of dopamine transporter as markers of disease burden. Methods: Seventy-eight subjects were included in this study (17 early de novo, 15 early l-dopa–treated, 24 moderate-advanced l-dopa–treated patients with PD, and 22 healthy controls). All participants underwent [11C]IMA107 PET, [11C]PE2I PET, and 3-Tesla MRI scan. Results: Early de novo PD patients showed loss of [11C]IMA107 and of [11C]PE2I binding in caudate and putamen (P < 0.001); early l-dopa–treated PD patients showed additional loss of [11C]IMA107 in the caudate (P < 0.001; annual decline 3.6%) and putamen (P < 0.001; annual decline 2.8%), but loss of [11C]PE2I only in the putamen (P < 0.001; annual decline 6.8%). Lower [11C]IMA107 correlated with lower [11C]PE2I in the caudate (rho = 0.51; P < 0.01) and putamen (rho = 0.53; P < 0.01). Longer disease duration correlated with lower [11C]IMA107 in the caudate (rho = –0.72; P < 0.001) and putamen (rho = –0.48; P < 0.01), and with lower [11C]PE2I only in the putamen (rho = –0.65; P < 0.001). Higher burden of motor symptoms correlated with lower [11C]IMA107 in the caudate (rho = –0.42; P < 0.05) and putamen (rho = –0.41; P < 0.05), and with lower [11C]PE2I only in the putamen (rho = –0.69; P < 0.001). Conclusion: Our findings demonstrate loss of phosphodiesterase 10A levels very early in the course of PD and is associated with the gradual and progressive increase of motor symptoms. Phosphodiesterase 10A imaging shows similar potential with dopamine transporter imaging to follow disease progression. © 2019 International Parkinson and Movement Disorder Society.
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Wilson H, Niccolini F, Pellicano C, Politis M (2019). Cortical thinning across Parkinson's disease stages and clinical correlates.
JOURNAL OF THE NEUROLOGICAL SCIENCES,
398, 31-38.
Author URL.
Wilson H, Pagano G, Politis M (2019). Dementia spectrum disorders: lessons learnt from decades with PET research.
JOURNAL OF NEURAL TRANSMISSION,
126(3), 233-251.
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Polychronis S, Dervenoulas G, Yousaf T, Niccolini F, Pagano G, Politis M (2019). Dysphagia is associated with presynaptic dopaminergic dysfunction and greater non-motor symptom burden in early drug-naive Parkinson's patients.
PLOS ONE,
14(7).
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Prakash N, Caspell-Garcia C, Coffey C, Siderowf A, Tanner CM, Kieburtz K, Mollenhauer B, Galasko D, Merchant K, Foroud T, et al (2019). Feasibility and safety of lumbar puncture in the Parkinson's disease research participants: Parkinson's Progression Marker Initiative (PPMI).
PARKINSONISM & RELATED DISORDERS,
62, 201-209.
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Wilson H, Dervenoulas G, Pagano G, Tyacke RJ, Polychronis S, Myers J, Gunn RN, Rabiner EA, Nutt D, Politis M, et al (2019). Imidazoline 2 binding sites reflecting astroglia pathology in Parkinson's disease: an in vivo11C-BU99008 PET study.
Brain,
142(10), 3116-3128.
Abstract:
Imidazoline 2 binding sites reflecting astroglia pathology in Parkinson's disease: an in vivo11C-BU99008 PET study.
Astroglia are multifunctional cells that regulate neuroinflammation and maintain homeostasis within the brain. Astroglial α-synuclein-positive cytoplasmic accumulations have been shown post-mortem in patients with Parkinson's disease and therefore astroglia may play an important role in the initiation and progression of Parkinson's disease. Imidazoline 2 binding sites are expressed on activated astroglia in the cortex, hippocampus, basal ganglia and brainstem; therefore, by measuring imidazoline 2 binding site levels we can indirectly evaluate astrogliosis in patients with Parkinson's disease. Here, we aimed to evaluate the role of astroglia activation in vivo in patients with Parkinson's disease using 11C-BU99008 PET, a novel radioligand with high specificity and selectivity for imidazoline 2 binding sites. Twenty-two patients with Parkinson's disease and 14 healthy control subjects underwent 3 T MRI and a 120-min 11C-BU99008 PET scan with volume of distribution (VT) estimated using a two-tissue compartmental model with a metabolite corrected arterial plasma input function. Parkinson's disease patients were stratified into early (n = 8) and moderate/advanced (n = 14) groups according to disease stage. In early Parkinson's disease, increased 11C-BU99008 VT uptake was observed in frontal (P = 0.022), temporal (P = 0.02), parietal (P = 0.026) and occipital (P = 0.047) cortical regions compared with healthy controls. The greatest 11C-BU99008 VT increase in patients with early Parkinson's disease was observed in the brainstem (52%; P = 0.018). In patients with moderate/advanced Parkinson's disease, loss of 11C-BU99008 VT was observed across frontal (P = 0.002), temporal (P < 0.001), parietal (P = 0.039), occipital (P = 0.024), and insula (P < 0.001) cortices; and in the subcortical regions of caudate (P < 0.001), putamen (P < 0.001) and thalamus (P < 0.001); and in the brainstem (P = 0.018) compared with healthy controls. In patients with Parkinson's disease, loss of 11C-BU99008 VT in cortical regions, striatum, thalamus and brainstem correlated with longer disease duration (P < 0.05) and higher disease burden scores, measured with Movement Disorder Society Unified Parkinson's Disease Rating Scale (P < 0.05). In the subgroup of patients with moderate/advanced Parkinson's disease, loss of 11C-BU99008 VT in the frontal (r = 0.79; P = 0.001), temporal (r = 0.74; P = 0.002) and parietal (r = 0.89; P < 0.001) cortex correlated with global cognitive impairment. This study demonstrates in vivo the role of astroglia in the initiation and progression of Parkinson's disease. Reactive astroglia observed early in Parkinson's disease could reflect a neuroprotective compensatory mechanisms and pro-inflammatory upregulation in response to α-synuclein accumulation. However, as the disease progresses and significant neurodegeneration occurs, astroglia lose their reactive function and such loss in the cortex has clinical relevance in the development of cognitive impairment.
Abstract.
Author URL.
Chandra A, Dervenoulas G, Politis M (2019). Magnetic resonance imaging in Alzheimer's disease and mild cognitive impairment.
JOURNAL OF NEUROLOGY,
266(6), 1293-1302.
Author URL.
Yousaf T, Dervenoulas G, Valkimadi P-E, Politis M (2019). Neuroimaging in Lewy body dementia.
JOURNAL OF NEUROLOGY,
266(1), 1-26.
Author URL.
Yousaf T, Pagano G, Niccolini F, Politis M (2019). Predicting cognitive decline with non-clinical markers in Parkinson's disease (PRECODE-2).
JOURNAL OF NEUROLOGY,
266(5), 1203-1210.
Author URL.
Wilson H, Dervenoulas G, Pagano G, Koros C, Yousaf T, Picillo M, Polychronis S, Simitsi A, Giordano B, Chappell Z, et al (2019). Serotonergic pathology and disease burden in the premotor and motor phase of A53T α-synuclein parkinsonism: a cross-sectional study.
LANCET NEUROLOGY,
18(8), 748-759.
Author URL.
Niccolini F, Wilson H, Giordano B, Diamantopoulos K, Pagano G, Chaudhuri KR, Politis M (2019). Sleep disturbances and gastrointestinal dysfunction are associated with thalamic atrophy in Parkinson's disease.
BMC Neuroscience,
20(1).
Abstract:
Sleep disturbances and gastrointestinal dysfunction are associated with thalamic atrophy in Parkinson's disease
Background: Non-motor symptoms are common aspects of Parkinson's disease (PD) occurring even at the prodromal stage of the disease and greatly affecting the quality of life. Here, we investigated whether non-motor symptoms burden was associated with cortical thickness and subcortical nuclei volume in PD patients. Methods: We studied 41 non-demented PD patients. Non-motor symptoms burden was assessed using the Non-Motor Symptoms Scale grading (NMSS). Cortical thickness and subcortical nuclei volume analyses were carried out using Free-Surfer. PD patients were divided into two groups according to the NMSS grading: Mild to moderate (NMSS: 0-40) and severe (NMSS: ≥ 41) non-motor symptoms. Results: Thalamic atrophy was associated with higher NMSQ and NMSS total scores. The non-motor symptoms that drove this correlation were sleep/fatigue and gastrointestinal tract dysfunction. We also found that PD patients with severe non-motor symptoms had significant thalamic atrophy compared to the group with mild to moderate non-motor symptoms. Conclusions: Our findings show that greater non-motor symptom burden is associated with thalamic atrophy in PD. Thalamus plays an important role in processing sensory information including visceral afferent from the gastrointestinal tract and in regulating states of sleep and wakefulness.
Abstract.
Polychronis S, Niccolini F, Pagano G, Yousaf T, Politis M (2019). Speech difficulties in early de novo patients with Parkinson's disease.
Parkinsonism and Related Disorders,
64, 256-261.
Abstract:
Speech difficulties in early de novo patients with Parkinson's disease
Introduction: Speech difficulties are a common debilitating feature of Parkinson's disease and we aimed to investigate whether speech difficulties are associated with striatal dopaminergic deficits and faster disease progression. Methods: Using the Parkinson's Progression Markers Initiative database, 143 early de novo Parkinson's disease patients with speech difficulties were identified and matched 1:1 with 143 Parkinson's disease patients without speech difficulties for age, disease duration and motor symptom severity. We investigated differences in clinical features and striatal [123I]FP-CIT single photon emission computed tomography (SPECT) uptake in Parkinson's disease patients with and without speech difficulties. Cox proportional hazards analysis was carried out to investigate whether speech difficulties were predictive of a faster motor progression and cognitive decline. Results: Speech difficulties were more common in patients with an akinetic-rigid motor phenotype compared to those with a tremor-dominant phenotype. Parkinson's disease patients with speech difficulties had lower resting tremor (P = 0.027), higher autonomic dysfunction (P = 0.034), increased daytime sleepiness (ESS; P = 0.048), and a higher prevalence of REM sleep behaviour disorder (RBD) symptoms (P = 0.007) compared to those without speech difficulties. Parkinson's disease patients with speech difficulties had significantly lower [123I]FP-CIT uptake in the striatum (P < 0.001), caudate (P = 0.003) and putamen (P = 0.003) compared to those without speech difficulties. The presence of speech difficulties was a predictor of cognitive decline [Hazard Ratio (HR): 0.341, 95% Confidence Interval (CI): 0.153–0.759; Wald: 6.945; P = 0.008), whereas it had no influence on motor progression (HR: 0.885, 95% CI: 0.662–1.183; Wald: 0.680; P > 0.10). Conclusion: Speech difficulties are associated with greater autonomic dysfunction, sleep disturbances and striatal dopaminergic deficit, and can serve as a predictor of faster cognitive decline in early Parkinson's disease.
Abstract.
Li W, Lao-Kaim NP, Roussakis AA, Martin-Bastida A, Valle-Guzman N, Paul G, Loane C, Widner H, Politis M, Foltynie T, et al (2018). <SUP>11</SUP>C-PE2I and <SUP>18</SUP>F-Dopa PET for Assessing Progression Rate in Parkinson's: a Longitudinal Study.
MOVEMENT DISORDERS,
33(1), 117-127.
Author URL.
Pagano G, Yousaf T, Wilson H, Niccolini F, Polychronis S, Chaudhuri KR, Politis M (2018). Constipation is not associated with dopamine transporter pathology in early drug-naïve patients with Parkinson's disease.
European Journal of Neurology,
25(2), 307-312.
Abstract:
Constipation is not associated with dopamine transporter pathology in early drug-naïve patients with Parkinson's disease
Background and purpose: Constipation is a common non-motor symptom of Parkinson's disease (PD). Deposition of α-synuclein inclusions that spread from the gut to the substantia nigra through the vagus nerve has recently been speculated to be a pre-motor and early stage of PD. The aim of the study was to investigate whether constipation is associated with dopaminergic pathology on dopamine transporter (DAT) single-photon emission computed tomography in early drug-naïve patients with PD. Our hypothesis was that constipation is associated with other signs of pre-motor PD and is independent of DAT pathology. We then investigated for associations with motor and non-motor symptoms, and with cerebrospinal fluid biomarkers of PD pathology. Methods: Using the Parkinson's Progression Markers Initiative database, we investigated the prevalence of constipation and the association between constipation and clinical features, striatal [123I]Ioflupane uptake and non-imaging (cerebrospinal fluid and serum) biomarkers. Constipation was evaluated using Movement Disorder Society-Sponsored Revision of the Unified Parkinson's Disease Rating Scale (MDS-UPDRS) Part I item 1.11. Results: One third (132/398) of de-novo patients with PD had constipation. Higher severity of constipation correlated with older age (r = 0.728, P < 0.001), higher MDS-UPDRS total score (r = 0.285, P < 0.001), worse postural instability (r = 0.190, P = 0.012), rapid eye movement sleep behaviour disorder (r = 0.228, P < 0.0001) and depression (r = 0.187, P = 0.024). No correlation was found with cerebrospinal fluid, serum and imaging markers of PD pathology. Conclusions: Constipation was not associated with DAT pathology but with rapid eye movement sleep behaviour disorder and depression, which are speculated to be pre-motor symptoms of PD. This confirms the hypothesis that constipation may be a pre-motor sign of PD due to an impairment of non-dopaminergic pathways.
Abstract.
Pagano G, Polychronis S, Wilson H, Giordano B, Ferrara N, Niccolini F, Politis M (2018). Diabetes mellitus and Parkinson disease.
NEUROLOGY,
90(19), E1654-E1662.
Author URL.
Niccolini F, Wilson H, Hirschbichler S, Yousaf T, Pagano G, Whittington A, Caminiti SP, Erro R, Holton JL, Jaunmuktane Z, et al (2018). Disease-related patterns of in vivo pathology in Corticobasal syndrome.
EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING,
45(13), 2413-2425.
Author URL.
Noyce AJ, Dickson J, Rees RN, Bestwick JP, Isaias IU, Politis M, Giovannoni G, Warner TT, Lees AJ, Schrag A, et al (2018). Dopamine Reuptake Transporter-Single-Photon Emission Computed Tomography and Transcranial Sonography as Imaging Markers of Prediagnostic Parkinson's Disease.
MOVEMENT DISORDERS,
33(3), 478-482.
Author URL.
Yousaf T, Pagano G, Niccolini F, Politis M (2018). Excessive daytime sleepiness may be associated with caudate denervation in Parkinson disease.
JOURNAL OF THE NEUROLOGICAL SCIENCES,
387, 220-227.
Author URL.
Strafella AP, Bohnen NI, Pavese N, Vaillancourt DE, van Eimeren T, Politis M, Tessitore A, Ghadery C, Lewis S (2018). Imaging Markers of Progression in Parkinson's Disease.
Movement Disorders Clinical Practice,
5(6), 586-596.
Abstract:
Imaging Markers of Progression in Parkinson's Disease
Background: Parkinson's disease (PD) is the second-most common neurodegenerative disorder after Alzheimer's disease; however, to date, there is no approved treatment that stops or slows down disease progression. Over the past decades, neuroimaging studies, including molecular imaging and MRI are trying to provide insights into the mechanisms underlying PD. Methods: This work utilized a literature review. Results: it is now becoming clear that these imaging modalities can provide biomarkers that can objectively detect brain changes related to PD and monitor these changes as the disease progresses, and these biomarkers are required to establish a breakthrough in neuroprotective or disease-modifying therapeutics. Conclusions: Here, we provide a review of recent observations deriving from PET, single-positron emission tomography, and MRI studies exploring PD and other parkinsonian disorders.
Abstract.
Yousaf T, Pagano G, Niccolini F, Politis M (2018). Increased dopaminergic function in the thalamus is associated with excessive daytime sleepiness.
SLEEP MEDICINE,
43, 25-30.
Author URL.
Yousaf T, Pagano G, Wilson H, Politis M (2018). Neuroimaging of Sleep Disturbances in Movement Disorders.
FRONTIERS IN NEUROLOGY,
9 Author URL.
Schulz J, Pagano G, Bonfante JAF, Wilson H, Politis M (2018). Nucleus basalis of Meynert degeneration precedes and predicts cognitive impairment in Parkinson's disease.
BRAIN,
141, 1501-1516.
Author URL.
Niccolini F, Mencacci NE, Yousaf T, Rabiner EA, Salpietro V, Pagano G, Balint B, Efthymiou S, Houlden H, Gunn RN, et al (2018). PDE10A and ADCY5 mutations linked to molecular and microstructural basal ganglia pathology.
MOVEMENT DISORDERS,
33(12), 1961-1965.
Author URL.
Hervé Du Penhoat MA, Moraga NR, Gaigeot MP, Vuilleumier R, Tavernelli I, Politis MF (2018). Proton Collision on Deoxyribose Originating from Doubly Ionized Water Molecule Dissociation.
Journal of Physical Chemistry A,
122(24), 5311-5320.
Abstract:
Proton Collision on Deoxyribose Originating from Doubly Ionized Water Molecule Dissociation
In this work, we studied the fragmentation dynamics of 2-deoxy-d-ribose (DR) in solution that arises from the double ionization of a water molecule in its primary hydration shell. This process was modeled in the framework of ab initio molecular dynamics. The charge unbalanced in the solvent molecules produces a Coulomb explosion with the consequent release of protons with kinetic energy in the few electronvolts range, which collide with the surrounding molecules in solution inducing further chemical reactions. In particular, we observe proton collisions with the solute molecule DR, which leads to a complete ring opening. In DNA, damage to the DR moiety may lead to DNA strand breaking. This mechanism can be understood as one of the possible steps in the radiation-induced fragmentation of DNA chains.
Abstract.
Pagano G, De Micco R, Yousaf T, Wilson H, Chandra A, Politis M (2018). REM behavior disorder predicts motor progression and cognitive decline in Parkinson disease.
NEUROLOGY,
91(10), E894-E905.
Author URL.
Wilson H, Giordano B, Turkheimer FE, Chaudhuri KR, Politis M (2018). Serotonergic dysregulation is linked to sleep problems in Parkinson's disease.
NEUROIMAGE-CLINICAL,
18, 630-637.
Author URL.
Niccolini F, Pagano G, Fusar-Poli P, Wood A, Mrzljak L, Sampaio C, Politis M (2018). Striatal molecular alterations in HD gene carriers: a systematic review and meta-analysis of PET studies.
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY,
89(2), 185-196.
Author URL.
Pagano G, Niccolini F, Politis M (2018). The serotonergic system in Parkinson's patients with dyskinesia: evidence from imaging studies.
JOURNAL OF NEURAL TRANSMISSION,
125(8), 1217-1223.
Author URL.
Politis M (2017). A systematic review of lessons learned from PET molecular imaging research in atypical parkinsonism (Niccolini and Politis, 2016).
EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING,
44(3), 548-550.
Author URL.
Politis M, Wilson H, Wu K, Brooks DJ, Piccini P (2017). Chronic exposure to dopamine agonists affects the integrity of striatal D<sub>2</sub> receptors in Parkinson's patients.
NEUROIMAGE-CLINICAL,
16, 455-460.
Author URL.
Aarsland D, Creese B, Politis M, Chaudhuri KR, Ffytche DH, Weintraub D, Ballard C (2017). Cognitive decline in Parkinson disease.
Nat Rev Neurol,
13(4), 217-231.
Abstract:
Cognitive decline in Parkinson disease.
Dementia is a frequent problem encountered in advanced stages of Parkinson disease (PD). In recent years, research has focused on the pre-dementia stages of cognitive impairment in PD, including mild cognitive impairment (MCI). Several longitudinal studies have shown that MCI is a harbinger of dementia in PD, although the course is variable, and stabilization of cognition - or even reversal to normal cognition - is not uncommon. In addition to limbic and cortical spread of Lewy pathology, several other mechanisms are likely to contribute to cognitive decline in PD, and a variety of biomarker studies, some using novel structural and functional imaging techniques, have documented in vivo brain changes associated with cognitive impairment. The evidence consistently suggests that low cerebrospinal fluid levels of amyloid-β42, a marker of comorbid Alzheimer disease (AD), predict future cognitive decline and dementia in PD. Emerging genetic evidence indicates that in addition to the APOE*ε4 allele (an established risk factor for AD), GBA mutations and SCNA mutations and triplications are associated with cognitive decline in PD, whereas the findings are mixed for MAPT polymorphisms. Cognitive enhancing medications have some effect in PD dementia, but no convincing evidence that progression from MCI to dementia can be delayed or prevented is available, although cognitive training has shown promising results.
Abstract.
Author URL.
Politis M (2017). Disease progression in <i>LRRK2</i> parkinsonism.
LANCET NEUROLOGY,
16(5), 334-335.
Author URL.
Moonga I, Niccolini F, Wilson H, Pagano G, Politis M (2017). Hypertension is associated with worse cognitive function and hippocampal hypometabolism in Alzheimer's disease.
European Journal of Neurology,
24(9), 1173-1182.
Abstract:
Hypertension is associated with worse cognitive function and hippocampal hypometabolism in Alzheimer's disease
Background and purpose: a growing body of evidence suggests that cardiovascular disease risk factors including hypertension may be linked to sporadic Alzheimer's disease (AD). It is well known that hypertension is associated with cerebrovascular disease and vascular dementia on the basis of vascular remodeling. However, the mechanisms linking hypertension and AD remain unclear. Methods: We studied 197 patients with AD (86 male; mean age ± SD: 75.8 ± 7.4 years) from the Alzheimer's Disease Neuroimaging Initiative database with (n = 97) and without (n = 100) hypertension. We explored associations between hypertension and clinical, plasma, cerebrospinal fluid and imaging markers of AD pathology in order to elucidate the underlying mechanisms that may link AD and hypertension. Results: We found that patients with AD with hypertension had worse cognitive function (Alzheimer's disease Assessment Scale-cognitive subscale, P = 0.038) and higher neuropsychiatric symptom burden (Neuropsychiatric Inventory Questionnaire, P = 0.016) compared with those without hypertension. Patients with AD with hypertension showed reduced glucose hypometabolism in the right (P < 0.001) and left (P = 0.007) hippocampus. No differences were found in magnetic resonance imaging volumetric measurements, [18F]florbetapir uptakes, plasma and cerebrospinal fluid between patients with AD with and without hypertension. Conclusions: Although hypertension is associated with worse cognitive function, behavioural symptoms and hippocampal glucose hypometabolism, it is not associated with evidence of increased amyloid or tau pathology. Effective management of hypertension may potentially have a therapeutic role in the alleviation of symptoms in AD.
Abstract.
Politis M, Lahiri N, Niccolini F, Su P, Wu K, Giannetti P, Scahill RI, Turkheimer FE, Tabrizi SJ, Piccini P, et al (2017). Increased central microglial activation associated with peripheral cytokine levels in premanifest Huntington's disease gene carriers (vol 83, pg 115, 2015).
NEUROBIOLOGY OF DISEASE,
98, 162-162.
Author URL.
Niccolini F, Wilson H, Pagano G, Coello C, Mehta MA, Searle GE, Gunn RN, Rabiner EA, Foltynie T, Politis M, et al (2017). Loss of phosphodiesterase 4 in Parkinson disease Relevance to cognitive deficits.
NEUROLOGY,
89(6), 586-593.
Author URL.
Wilson H, De Micco R, Niccolini F, Politis M (2017). Molecular imaging Markers to Track Huntington's Disease Pathology.
FRONTIERS IN NEUROLOGY,
8 Author URL.
Strafella AP, Bohnen NI, Perlmutter JS, Eidelberg D, Pavese N, Van Eimeren T, Piccini P, Politis M, Thobois S, Ceravolo R, et al (2017). Molecular imaging to track Parkinson's disease and atypical parkinsonisms: New imaging frontiers.
MOVEMENT DISORDERS,
32(2), 181-192.
Author URL.
Martin-Bastida A, Lao-Kaim NP, Loane C, Politis M, Roussakis AA, Valle-Guzman N, Kefalopoulou Z, Paul-Visse G, Widner H, Xing Y, et al (2017). Motor associations of iron accumulation in deep grey matter nuclei in Parkinson's disease: a cross-sectional study of iron-related magnetic resonance imaging susceptibility.
European Journal of Neurology,
24(2), 357-365.
Abstract:
Motor associations of iron accumulation in deep grey matter nuclei in Parkinson's disease: a cross-sectional study of iron-related magnetic resonance imaging susceptibility
Background and purpose: to determine whether iron deposition in deep brain nuclei assessed using high-pass filtered phase imaging plays a role in motor disease severity in Parkinson's disease (PD). Methods: Seventy patients with mild to moderate PD and 20 age- and gender-matched healthy volunteers (HVs) underwent susceptibility-weighted imaging on a 3 T magnetic resonance imaging scanner. Phase shifts (radians) in deep brain nuclei were derived from high-pass filtered phase images and compared between groups. Analysis of clinical laterality and correlations with motor severity (Unified Parkinson's Disease Rating Scale, Part III, UPDRS-III) were performed. Phase shifts (in radians) were compared between HVs and three PD subgroups divided according to UPDRS-III scores using analysis of covariance, adjusting for age and regional area. Results: Parkinson's disease patients had significantly (P < 0.001) higher radians than HVs bilaterally in the putamen, globus pallidus and substantia nigra (SN). The SN contralateral to the most affected side showed higher radians (P < 0.001) compared to the less affected side. SN radians positively correlated with UPDRS-III and bradykinesia−rigidity subscores, but not with tremor subscores. ancova followed by post hoc Bonferroni-adjusted pairwise comparisons revealed that SN radians were significantly greater in the PD subgroup with higher UPDRS-III scores compared to both lowest UPDRS-III PD and HV groups (P < 0.001). Conclusions: Increased nigral iron accumulation in PD appears to be stratified according to disease motor severity and correlates with symptoms related to dopaminergic neurodegeneration. This semi-quantitative in vivo iron assessment could prove useful for objectively monitoring PD progression, especially in clinical trials concerning iron chelation therapies.
Abstract.
Pagano G, Yousaf T, Politis M (2017). PET Molecular Imaging Research of Levodopa-Induced Dyskinesias in Parkinson's Disease.
CURRENT NEUROLOGY AND NEUROSCIENCE REPORTS,
17(11).
Author URL.
Mehranian A, Belzunce MA, Niccolini F, Politis M, Prieto C, Turkheimer F, Hammers A, Reader AJ (2017). PET image reconstruction using multi-parametric anato-functional priors.
PHYSICS IN MEDICINE AND BIOLOGY,
62(15), 5975-6007.
Author URL.
Qamar MA, Sauerbier A, Politis M, Carr H, Loehrer P, Chaudhuri KR (2017). Presynaptic dopaminergic terminal imaging & non-motor symptoms assessment of Parkinson's disease: Evidence for dopaminergic basis?.
Parkinson's Disease,
3(1).
Abstract:
Presynaptic dopaminergic terminal imaging & non-motor symptoms assessment of Parkinson's disease: Evidence for dopaminergic basis?
Parkinson's disease (PD) is now considered to be a multisystemic disorder consequent on multineuropeptide dysfunction including dopaminergic, serotonergic, cholinergic, and noradrenergic systems. This multipeptide dysfunction leads to expression of a range of non-motor symptoms now known to be integral to the concept of PD and preceding the diagnosis of motor PD. Some nonmotor symptoms in PD may have a dopaminergic basis and in this review, we investigate the evidence for this based on imaging techniques using dopamine-based radioligands. To discuss non-motor symptoms we follow the classification as outlined by the validated PD non-motor symptoms scale.
Abstract.
Pagano G, Niccolini F, Fusar-Poli P, Politis M (2017). Serotonin transporter in Parkinson's disease: a meta-analysis of positron emission tomography studies.
ANNALS OF NEUROLOGY,
81(2), 171-180.
Author URL.
Politis M, Sauerbier A, Loane C, Pavese N, Martin A, Corcoran B, Brooks DJ, Ray-Chaudhuri K, Piccini P (2017). Sustained striatal dopamine levels following intestinal levodopa infusions in Parkinson's disease patients.
MOVEMENT DISORDERS,
32(2), 235-240.
Author URL.
Ffytche DH, Creese B, Politis M, Chaudhuri KR, Weintraub D, Ballard C, Aarsland D (2017). The psychosis spectrum in Parkinson disease.
Nat Rev Neurol,
13(2), 81-95.
Abstract:
The psychosis spectrum in Parkinson disease.
In 2007, the clinical and research profile of illusions, hallucinations, delusions and related symptoms in Parkinson disease (PD) was raised with the publication of a consensus definition of PD psychosis. Symptoms that were previously deemed benign and clinically insignificant were incorporated into a continuum of severity, leading to the rapid expansion of literature focusing on clinical aspects, mechanisms and treatment. Here, we review this literature and the evolving view of PD psychosis. Key topics include the prospective risk of dementia in individuals with PD psychosis, and the causal and modifying effects of PD medication. We discuss recent developments, including recognition of an increase in the prevalence of psychosis with disease duration, addition of new visual symptoms to the psychosis continuum, and identification of frontal executive, visual perceptual and memory dysfunction at different disease stages. In addition, we highlight novel risk factors - for example, autonomic dysfunction - that have emerged from prospective studies, structural MRI evidence of frontal, parietal, occipital and hippocampal involvement, and approval of pimavanserin for the treatment of PD psychosis. The accumulating evidence raises novel questions and directions for future research to explore the clinical management and biomarker potential of PD psychosis.
Abstract.
Author URL.
Pagano G, Niccolini F, Yousaf T, Wilson H, Polychronis S, Chaudhuri KR, Politis M (2017). Urinary Dysfunction in Early De Novo Patients with Parkinson's Disease.
MOVEMENT DISORDERS,
32(6), 939-940.
Author URL.
Niccolini F, Politis M (2016). A systematic review of lessons learned from PET molecular imaging research in atypical parkinsonism.
EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING,
43(12), 2244-2254.
Author URL.
Loane C, Politis M, Kefalopoulou Z, Valle-Guzman N, Paul G, Widner H, Foltynie T, Barker RA, Piccini P (2016). Aberrant nigral diffusion in Parkinson's disease: a longitudinal diffusion tensor imaging study.
MOVEMENT DISORDERS,
31(7), 1020-1026.
Author URL.
Diggle CP, Sukoff Rizzo SJ, Popiolek M, Hinttala R, Schülke J-P, Kurian MA, Carr IM, Markham AF, Bonthron DT, Watson C, et al (2016). Biallelic Mutations in PDE10A Lead to Loss of Striatal PDE10A and a Hyperkinetic Movement Disorder with Onset in Infancy.
Am J Hum Genet,
98(4), 735-743.
Abstract:
Biallelic Mutations in PDE10A Lead to Loss of Striatal PDE10A and a Hyperkinetic Movement Disorder with Onset in Infancy.
Deficits in the basal ganglia pathways modulating cortical motor activity underlie both Parkinson disease (PD) and Huntington disease (HD). Phosphodiesterase 10A (PDE10A) is enriched in the striatum, and animal data suggest that it is a key regulator of this circuitry. Here, we report on germline PDE10A mutations in eight individuals from two families affected by a hyperkinetic movement disorder due to homozygous mutations c.320A>G (p.Tyr107Cys) and c.346G>C (p.Ala116Pro). Both mutations lead to a reduction in PDE10A levels in recombinant cellular systems, and critically, positron-emission-tomography (PET) studies with a specific PDE10A ligand confirmed that the p.Tyr107Cys variant also reduced striatal PDE10A levels in one of the affected individuals. A knock-in mouse model carrying the homologous p.Tyr97Cys variant had decreased striatal PDE10A and also displayed motor abnormalities. Striatal preparations from this animal had an impaired capacity to degrade cyclic adenosine monophosphate (cAMP) and a blunted pharmacological response to PDE10A inhibitors. These observations highlight the critical role of PDE10A in motor control across species.
Abstract.
Author URL.
Roy R, Niccolini F, Pagano G, Politis M (2016). Cholinergic imaging in dementia spectrum disorders.
EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING,
43(7), 1376-1386.
Author URL.
Pagano G, Niccolini F, Politis M (2016). Current status of PET imaging in Huntington's disease.
EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING,
43(6), 1171-1182.
Author URL.
Sauerbier A, Martinez-Martin P, Politis M, Rizos A, Trojanovic N, Mulholland N, Vivian G, Corcoran B, Trivedi D, Perkins L, et al (2016). Fatigue in Parkinson's disease and striatum dopamine transporter scan (DaTscan) uptake. Parkinsonism & Related Disorders, 22
Sauerbier A, Martinez-Martin P, Politis M, Rizos A, Trojanovic N, Mulholland N, Vivian G, Corcoran B, Trivedi D, Perkins L, et al (2016). Fatigue in Parkinson's disease and striatum dopamine transporter scan (DaTscan) uptake. Parkinsonism & Related Disorders, 22, e161-e162.
Pagano G, Niccolini F, Politis M (2016). Imaging in Parkinson's disease.
CLINICAL MEDICINE,
16(4), 371-375.
Author URL.
Wilson H, Niccolini F, Haider S, Marques TR, Pagano G, Coello C, Natesan S, Kapur S, Rabiner EA, Gunn RN, et al (2016). Loss of extra-striatal phosphodiesterase 10A expression in early premanifest Huntington's disease gene carriers.
JOURNAL OF THE NEUROLOGICAL SCIENCES,
368, 243-248.
Author URL.
Politis M, Ashraghi M, Pagano G, Polychronis S, Niccolini F (2016). Parkinson’s Disease, Diabetes and Cognitive Impairment. Recent Patents on Endocrine Metabolic & Immune Drug Discovery, 10(999), 1-1.
Ashraghi MR, Pagano G, Polychronis S, Niccolini F, Politis M (2016). Parkinson’s disease, diabetes and cognitive impairment.
Recent Patents on Endocrine, Metabolic and Immune Drug Discovery,
10(1), 11-21.
Abstract:
Parkinson’s disease, diabetes and cognitive impairment
Background: Parkinson’s disease is a chronic neurodegenerative disorder characterized by a progressive loss of dopaminergic neurons. The pathophysiological mechanisms underlying Parkinson’s are still unknown. Mitochondrial dysfunction, abnormal protein aggregation, increased neuroinflammation and impairment of brain glucose metabolism are shared processes among insulinresistance, diabetes and neurodegeneration and have been suggested as key mechanisms in development of Parkinson’s and cognitive impairment. Objective: to review experimental and clinical evidence of underlying Parkinson’s pathophysiology in common with diabetes and cognitive impairment. Anti-diabetic agents and recent patents for insulin-resistance that might be repositioned in the treatment of Parkinson’s also have been included in this review. Method: a narrative review using MEDLINE database. Results: Common antidiabetic treatments such as DPP4 inhibitors, GLP-1 agonists and metformin have shown promise in the treatment of Parkinson’s disease and cognitive impairment in animals and humans. Study of the pathophysiology of neurodegeneration common between diabetes and Parkinson’s disease has given rise to new treatment possibilities. Patents published in the last 5 years could be used in novel approaches to Parkinson’s treatment by targeting specific pathophysiology proteins, such as Nurr1, PINK1 and NrF2, while patents to improve penetration of the blood brain barrier could allow improved efficacy of existing treatments. Conclusion: Further studies using GLP-1 agonists and DPP-4 inhibitors to treat PD are warranted as they have shown promise.
Abstract.
Marques TR, Natesan S, Niccolini F, Politis M, Gunn RN, Searle GE, Howes O, Rabiner EA, Kapur S (2016). Phosphodiesterase 10A in Schizophrenia: a PET Study Using [<SUP>11</SUP>C]IMA107.
AMERICAN JOURNAL OF PSYCHIATRY,
173(7), 714-721.
Author URL.
Schrag A, Politis M (2016). Serotonergic loss underlying apathy in Parkinson's disease.
BRAIN,
139, 2338-2339.
Author URL.
Roussakis A-A, Politis M, Towey D, Piccini P (2016). Serotonin-to-dopamine transporter ratios in Parkinson disease Relevance for dyskinesias.
NEUROLOGY,
86(12), 1152-1158.
Author URL.
Niccolini F, Haider S, Marques TR, Muhlert N, Tziortzi AC, Searle GE, Natesan S, Piccini P, Kapur S, Rabiner EA, et al (2015). Altered PDE10A expression detectable early before symptomatic onset in Huntington's disease.
BRAIN,
138, 3016-3029.
Author URL.
Giannetti P, Politis M, Su P, Turkheimer FE, Malik O, Keihaninejad S, Wu K, Waldman A, Reynolds R, Nicholas R, et al (2015). Increased PK11195-PET binding in normal-appearing white matter in clinically isolated syndrome.
BRAIN,
138, 110-119.
Author URL.
Politis M, Lahiri N, Niccolini F, Su P, Wu K, Giannetti P, Scahill RI, Turkheimer FE, Tabrizi SJ, Piccini P, et al (2015). Increased central microglial activation associated with peripheral cytokine levels in premanifest Huntington's disease gene carriers.
NEUROBIOLOGY OF DISEASE,
83, 115-121.
Author URL.
Niccolini F, Foltynie T, Marques TR, Muhlert N, Tziortzi AC, Searle GE, Natesan S, Kapur S, Rabiner EA, Gunn RN, et al (2015). Loss of phosphodiesterase 10A expression is associated with progression and severity in Parkinson's disease.
BRAIN,
138, 3003-3015.
Author URL.
Niccolini F, Rocchi L, Politis M (2015). Molecular imaging of levodopa-induced dyskinesias.
CELLULAR AND MOLECULAR LIFE SCIENCES,
72(11), 2107-2117.
Author URL.
Pellicano C, Niccolini F, Wu K, O'Sullivan SS, Lawrence AD, Lees AJ, Piccini P, Politis M (2015). Morphometric changes in the reward system of Parkinson's disease patients with impulse control disorders.
JOURNAL OF NEUROLOGY,
262(12), 2653-2661.
Author URL.
Niccolini F, Su P, Politis M (2015). PET in Multiple Sclerosis.
CLINICAL NUCLEAR MEDICINE,
40(1), E46-E52.
Author URL.
Loane C, Wu K, O'Sullivan SS, Lawrence AD, Woodhead Z, Lees AJ, Piccini P, Politis M (2015). Psychogenic and neural visual-cue response in PD dopamine dysregulation syndrome.
PARKINSONISM & RELATED DISORDERS,
21(11), 1336-1341.
Author URL.
Rocchi L, Niccolini F, Politis M (2015). Recent imaging advances in neurology.
JOURNAL OF NEUROLOGY,
262(9), 2182-2194.
Author URL.
Politis M, Niccolini F (2015). Serotonin in Parkinson's disease.
Behav Brain Res,
277, 136-145.
Abstract:
Serotonin in Parkinson's disease.
Parkinson's disease is a chronic neurodegenerative disorder characterized by the motor symptoms of bradykinesia, tremor, rigidity and postural instability. However, non-motor symptoms such as chronic fatigue, depression, dementia and sleep disturbances are also frequent and play a significant role with negative consequences in the quality of life of patients with Parkinson's disease. Although the progressive dopaminergic denervation is the cardinal pathology in the brains of patients with Parkinson's disease, others systems such as the serotonergic are affected as well. Over the last decade, several lines of evidence suggest that a progressive and non-linear loss of serotonergic terminals takes place in Parkinson's disease, though this is at a slower pace compared to the dopaminergic loss. Several studies have indicated that serotonergic dysfunction in Parkinson's disease is associated with the development of motor and non-motor symptoms and complications. Here, we aim to review the current evidence with regards to the serotonergic pathology in Parkinson's disease and its relevance to the development of clinical symptoms. We are primarily revising in vivo human studies from research with positron emission tomography molecular imaging.
Abstract.
Author URL.
Wu K, Politis M, O'Sullivan SS, Lawrence AD, Warsi S, Bose S, Lees AJ, Piccini P (2015). Single versus multiple impulse control disorders in Parkinson's disease: an <SUP>11</SUP>C-raclopride positron emission tomography study of reward cue-evoked striatal dopamine release.
JOURNAL OF NEUROLOGY,
262(6), 1504-1514.
Author URL.
Turkheimer FE, Bodini B, Politis M, Pariante CM, Ciccarelli O, Yeo RA (2015). The X-Linked Hypothesis of Brain Disorders: can Gender Ratios Tell Us Anything About Cellular Etiology of Neurodegenerative and Psychiatric Diseases?.
NEUROSCIENTIST,
21(6), 589-598.
Author URL.
Smith R, Wu K, Hart T, Loane C, Brooks DJ, Bjorklund A, Odin P, Piccini P, Politis M (2015). The role of pallidal serotonergic function in Parkinson's disease dyskinesias: a positron emission tomography study.
NEUROBIOLOGY OF AGING,
36(4), 1736-1742.
Author URL.
Niccolini F, Su P, Politis M (2014). Dopamine receptor mapping with PET imaging in Parkinson's disease.
JOURNAL OF NEUROLOGY,
261(12), 2251-2263.
Author URL.
Niccolini F, Loane C, Politis M (2014). Dyskinesias in Parkinson's disease: views from positron emission tomography studies.
EUROPEAN JOURNAL OF NEUROLOGY,
21(5), 694-+.
Author URL.
Garvey LJ, Pavese N, Politis M, Ramlackhansingh A, Brooks DJ, Taylor-Robinson SD, Winston A (2014). Increased microglia activation in neurologically asymptomatic HIV-infected patients receiving effective ART.
AIDS,
28(1), 67-72.
Author URL.
Kefalopoulou Z, Politis M, Piccini P, Mencacci N, Bhatia K, Jahanshahi M, Widner H, Rehncrona S, Brundin P, Bjorklund A, et al (2014). Long-term Clinical Outcome of Fetal Cell Transplantation for Parkinson Disease Two Case Reports.
JAMA NEUROLOGY,
71(1), 83-87.
Author URL.
Giannetti P, Politis M, Su P, Turkheimer F, Malik O, Keihaninejad S, Wu K, Reynolds R, Nicholas R, Piccini P, et al (2014). Microglia activation in multiple sclerosis black holes predicts outcome in progressive patients: an in vivo [(11)C](R)-PK11195-PET pilot study.
NEUROBIOLOGY OF DISEASE,
65, 203-210.
Author URL.
Niccolini F, Politis M (2014). Neuroimaging in Huntington's disease.
World J Radiol,
6(6), 301-312.
Abstract:
Neuroimaging in Huntington's disease.
Huntington's disease (HD) is a progressive and fatal neurodegenerative disorder caused by an expanded trinucleotide CAG sequence in huntingtin gene (HTT) on chromosome 4. HD manifests with chorea, cognitive and psychiatric symptoms. Although advances in genetics allow identification of individuals carrying the HD gene, much is still unknown about the mechanisms underlying the development of overt clinical symptoms and the transitional period between premanifestation and manifestation of the disease. HD has no cure and patients rely only in symptomatic treatment. There is an urgent need to identify biomarkers that are able to monitor disease progression and assess the development and efficacy of novel disease modifying drugs. Over the past years, neuroimaging techniques such as magnetic resonance imaging (MRI) and positron emission tomography (PET) have provided important advances in our understanding of HD. MRI provides information about structural and functional organization of the brain, while PET can detect molecular changes in the brain. MRI and PET are able to detect changes in the brains of HD gene carriers years ahead of the manifestation of the disease and have also proved to be powerful in assessing disease progression. However, no single technique has been validated as an optimal biomarker. An integrative multimodal imaging approach, which combines different MRI and PET techniques, could be recommended for monitoring potential neuroprotective and preventive therapies in HD. In this article we review the current neuroimaging literature in HD.
Abstract.
Author URL.
Politis M (2014). Neuroimaging in Parkinson disease: from research setting to clinical practice.
NATURE REVIEWS NEUROLOGY,
10(12), 708-722.
Author URL.
Wu K, Politis M, O'Sullivan SS, Lawrence AD, Warsi S, Lees A, Piccini P (2014). Problematic Internet use in Parkinson's disease.
PARKINSONISM & RELATED DISORDERS,
20(5), 482-487.
Author URL.
Politis M, Wu K, Loane C, Brooks DJ, Kiferle L, Turkheimer FE, Bain P, Molloy S, Piccini P (2014). Serotonergic mechanisms responsible for levodopa-induced dyskinesias in Parkinson's disease patients.
JOURNAL OF CLINICAL INVESTIGATION,
124(3), 1340-1349.
Author URL.
Loane C, Pilinis C, Lekkas TD, Politis M (2013). Ambient particulate matter and its potential neurological consequences.
REVIEWS IN THE NEUROSCIENCES,
24(3), 323-335.
Author URL.
Roussakis A-A, Piccini P, Politis M (2013). Clinical utility of DaTscan™ (123I-Ioflupane Injection) in the diagnosis of Parkinsonian Syndromes.
Degener Neurol Neuromuscul Dis,
3, 33-39.
Abstract:
Clinical utility of DaTscan™ (123I-Ioflupane Injection) in the diagnosis of Parkinsonian Syndromes.
The diagnosis of movement disorders including Parkinsonian syndromes and essential tremor is mainly clinical. The most common diagnostic errors for Parkinson's disease include misdiagnoses such as Parkinson plus syndromes and cases of essential tremor. In this article, we discuss the clinical utility of DaTscan™ (123I-Ioflupane injection) and its diagnostic value in Parkinson's disease and the other Parkinsonian syndromes. Single photon emission computed tomography with 123I-Ioflupane can be useful to assist in the diagnosis of uncertain cases of Parkinsonism. An accurate diagnosis can aid clinicians in making correct decisions that are related to the overall management and treatment of Parkinson's disease, avoiding common therapeutic errors.
Abstract.
Author URL.
O'Sullivan SS, Wu K, Politis M, Lawrence AD, Evans AH, Bose SK, Djamshidian A, Lees AJ, Piccini P (2013). Cue-induced striatal dopamine release in Parkinson's disease-associated impulsive-compulsive behaviours (vol 134, pg 969, 2011).
BRAIN,
136, 985-985.
Author URL.
Politis M, Loane C, Wu K, O'Sullivan SS, Woodhead Z, Kiferle L, Lawrence AD, Lees AJ, Piccini P (2013). Neural response to visual sexual cues in dopamine treatment-linked hypersexuality in Parkinson's disease.
BRAIN,
136, 400-411.
Author URL.
Loane C, Wu K, Bain P, Brooks DJ, Piccini P, Politis M (2013). Serotonergic loss in motor circuitries correlates with severity of action-postural tremor in PD.
NEUROLOGY,
80(20), 1850-1855.
Author URL.
Garvey LJ, Pavese N, Ramlackhansingh A, Thomson E, Allsop JM, Politis M, Kulasegaram R, Main J, Brooks DJ, Taylor-Robinson SD, et al (2012). Acute HCV/HIV Coinfection is Associated with Cognitive Dysfunction and Cerebral Metabolite Disturbance, but Not Increased Microglial Cell Activation.
PLOS ONE,
7(7).
Author URL.
Loane C, Politis M (2012). Buspirone: What is it all about?.
BRAIN RESEARCH,
1461, 111-118.
Author URL.
Politis M, Lindvall O (2012). Clinical application of stem cell therapy in Parkinson's disease.
BMC MEDICINE,
10 Author URL.
Politis M, Su P, Piccini P (2012). Imaging of microglia in patients with neurodegenerative disorders.
FRONTIERS IN PHARMACOLOGY,
3 Author URL.
Wu K, Politis M, Piccini P (2012). Impulse control disorders in parkinson's disease: a review.
Current Psychiatry Reviews,
8(3), 235-246.
Abstract:
Impulse control disorders in parkinson's disease: a review
The development of Impulse Control Disorders (ICDs) in Parkinson's disease (PD) is a recognised iatrogenic complication associated with the use of dopamine agonists. The prevalence of ICDs has been reported to be as high as 14% in studies conducted in Europe and North America. Early case reports and recent large-scale studies have shown that clinical features associated with the development of PD-related ICDs include novelty-seeking personality traits, early onset PD and a past history of psychiatric conditions. More recent studies have also suggested that ICDs may be associated with deep brain stimulation and dyskinesias. Moreover, there is heterogeneity in the clinical features associated with the range of ICDs, with studies pointing out that compulsive sexual behaviours and binge eating have fewer clinical features in common than compulsive buying and pathological gambling. The recent increase in the number of functional neuroimaging studies on patients with PD and ICDs, particularly those with pathological gambling, has provided a unique opportunity to understand the neurobiology of the disorder, and has indicated an abnormality in the meso-limbic dopaminergic pathways. Further studies directly comparing ICD sufferers with and without PD will provide valuable knowledge to aid in the management of both patient groups. This review will provide a clinical overview of impulse control behaviours in PD, including both commonly reported ICDs and other related impulsive-compulsive behaviours observed in PD. © 2012 Bentham Science Publishers.
Abstract.
Politis M, Giannetti P, Su P, Turkheimer F, Keihaninejad S, Wu K, Waldman A, Malik O, Matthews PM, Reynolds R, et al (2012). Increased PK11195 PET binding in the cortex of patients with MS correlates with disability.
NEUROLOGY,
79(6), 523-530.
Author URL.
Politis M, Piccini P (2012). Positron emission tomography imaging in neurological disorders.
JOURNAL OF NEUROLOGY,
259(9), 1769-1780.
Author URL.
Politis M, Loane C (2012). Reduplicative Paramnesia: a Review.
PSYCHOPATHOLOGY,
45(6), 337-343.
Author URL.
Politis M, Wu K, Loane C, Quinn NP, Brooks DJ, Oertel WH, Bjorklund A, Lindvall O, Piccini P (2012). Serotonin Neuron Loss and Nonmotor Symptoms Continue in Parkinson's Patients Treated with Dopamine Grafts.
SCIENCE TRANSLATIONAL MEDICINE,
4(128).
Author URL.
Wu K, O'Keeffe D, Politis M, O'Keeffe GC, Robbins TW, Bose SK, Brooks DJ, Piccini P, Barker RA (2012). The catechol-O-methyltransferase Val<SUP>158</SUP>Met polymorphism modulates fronto-cortical dopamine turnover in early Parkinson's disease: a PET study.
BRAIN,
135, 2449-2457.
Author URL.
O'Sullivan SS, Wu K, Politis M, Lawrence AD, Evans AH, Bose SK, Djamshidian A, Lees AJ, Piccini P (2011). Cue-induced striatal dopamine release in Parkinson's disease-associated impulsive-compulsive behaviours.
BRAIN,
134, 969-978.
Author URL.
Loane C, Su P, Politis M (2011). Different dyskinesias in Parkinson's disease and their relationship to levodopa.
European Neurological Journal,
3(1), 20-26.
Abstract:
Different dyskinesias in Parkinson's disease and their relationship to levodopa
Levodopa is the principal agent in the treatment of Parkinson's disease (PD). Unfortunately the therapeutic benefits are optimal only in the early stages of the disease, with long-term use associated with motor complications such as levodopa-induced dyskinesia (LID). Risk factors associated with the development of LID are generally accepted to involve the degree of dopamine (DA) denervation in the nigrostriatal pathway, levodopa dose, and duration of levodopa treatment. Little is known regarding the underlying mechanisms of LID, although it is known that levodopa plasma concentrations are closely associated with the onset of some types of LIDs (peak-dose and biphasic dyskinesias) and it appears that increased DA turnover plays a crucial role in LID development. Recent evidence suggests that other cell types such as serotonin neurons possess the ability to convert levodopa into DA, subsequently storing and releasing it thereby increasing the levels of extracellular DA, exacerbating LID. This review will highlight the evidence to date from in vitro and in vivo studies utilizing both animal models and patients, regarding the relationship between levodopa treatment and the development of LID. Understanding the pathogenesis of LID is a therapeutic priority in tackling motor complications related to levodopa treatment in PD.
Abstract.
Politis M, Oertel WH, Wu K, Quinn NP, Pogarell O, Brooks DJ, Bjorklund A, Lindvall O, Piccini P (2011). Graft-Induced Dyskinesias in Parkinson's Disease: High Striatal Serotonin/Dopamine Transporter Ratio.
MOVEMENT DISORDERS,
26(11), 1997-2003.
Author URL.
Politis M, Pavese N, Tai YF, Kiferle L, Mason SL, Brooks DJ, Tabrizi SJ, Barker RA, Piccini P (2011). Microglial activation in regions related to cognitive function predicts disease onset in Huntington's Disease: a multimodal imaging study.
HUMAN BRAIN MAPPING,
32(2), 258-270.
Author URL.
Politis M (2011). Optimizing functional imaging protocols for assessing the outcome of fetal cell transplantation in Parkinson's disease.
BMC MEDICINE,
9 Author URL.
Kiferle L, Politis M, Muraro PA, Piccini P (2011). Positron emission tomography imaging in multiple sclerosis-current status and future applications.
EUROPEAN JOURNAL OF NEUROLOGY,
18(2), 226-231.
Author URL.
Loane C, Politis M (2011). Positron emission tomography neuroimaging in Parkinson's disease.
AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH,
3(4), 323-341.
Author URL.
Politis M, Loane C (2011). Serotonergic Dysfunction in Parkinson's Disease and its Relevance to Disability.
THESCIENTIFICWORLDJOURNAL,
11, 1726-1734.
Author URL.
Politis M, Loane C, Wu K, Brooks DJ, Piccini P (2011). Serotonergic mediated body mass index changes in Parkinson's disease.
NEUROBIOLOGY OF DISEASE,
43(3), 609-615.
Author URL.
Su P, Loane C, Politis M (2011). The Use of Stem Cells in the Treatment of Parkinsons Disease. Insciences Journal, 136-156.
Politis M, Piccini P (2010). Brain imaging after neural transplantation.
Prog Brain Res,
184, 193-203.
Abstract:
Brain imaging after neural transplantation.
Functional imaging has provided objective evidence that human fetal ventral mesencephalic tissue implanted in the striatum of Parkinson's disease patients can survive, grow, release dopamine, normalize brain metabolism, and restore striatal-cortical connections. Open-label clinical trials have shown robust clinical improvement in several PD patients but these results were not replicated in two double-blind sham-surgery controlled clinical trials. Graft-induced dyskinesias are serious adverse effects and a major roadblock for the further development of cell therapies, and functional imaging can help investigate the mechanisms underlying their cause. Functional imaging can also aid future trials by improving patient selection, assessing restoration of brain connectivity, and monitor inflammatory processes. Although functional imaging cannot currently be used as a primary endpoint in clinical transplantation trials, it can provide additional valuable information alongside clinical observations.
Abstract.
Author URL.
Pavese N, Politis M, Tai YF, Barker RA, Tabrizi SJ, Mason SL, Brooks DJ, Piccini P (2010). Cortical dopamine dysfunction in symptomatic and premanifest Huntington's disease gene carriers.
NEUROBIOLOGY OF DISEASE,
37(2), 356-361.
Author URL.
Politis M, Wu K, Loane C, Turkheimer FE, Molloy S, Brooks DJ, Piccini P (2010). Depressive symptoms in PD correlate with higher 5-HTT binding in raphe and limbic structures.
NEUROLOGY,
75(21), 1920-1927.
Author URL.
Politis M (2010). Dyskinesias after neural transplantation in Parkinson's disease: what do we know and what is next?.
BMC MEDICINE,
8 Author URL.
Politis M, Wu K, Molloy S, Bain PG, Chaudhuri KR, Piccini P (2010). Parkinson's Disease Symptoms: the Patient's Perspective.
MOVEMENT DISORDERS,
25(11), 1646-1651.
Author URL.
Politis M, Wu K, Loane C, Quinn NP, Brooks DJ, Rehncrona S, Bjorklund A, Lindvall O, Piccini P (2010). Serotonergic Neurons Mediate Dyskinesia Side Effects in Parkinson's Patients with Neural Transplants.
SCIENCE TRANSLATIONAL MEDICINE,
2(38).
Author URL.
Politis M, Wu K, Loane C, Kiferle L, Molloy S, Brooks DJ, Piccini P (2010). Staging of serotonergic dysfunction in Parkinson's Disease: an <i>in vivo</i> <SUP>11</SUP>C-DASB PET study.
NEUROBIOLOGY OF DISEASE,
40(1), 216-221.
Author URL.
Wu K, Politis M, Piccini P (2009). Parkinson disease and impulse control disorders: a review of clinical features, pathophysiology and management.
POSTGRADUATE MEDICAL JOURNAL,
85(1009), 590-596.
Author URL.
Politis M, Wu K, Piccini P (2009). Positron emission tomography imaging in Parkinson's disease.
Minerva Psichiatrica,
50(1), 55-78.
Abstract:
Positron emission tomography imaging in Parkinson's disease
Positron emission tomography (PET) neurolmaging techniques provide a useful tool for understanding the complex functional anatomy of the basal ganglia and their disorders. They help to elucidate the pathophysiological mechanisms underlying the degenerative processes and the evolution of symptoms in Parkinson's disease (PD). In this review, the potential role of PET imaging on evaluating the dopaminerglc and non-dopaminergic function in PD is discussed along with its use as a biological marker in the differential diagnosis of typical and atypical parklnsonism, in monitoring disease's progression, and in understanding the mechanisms underlying motor fluctuations, dnig induced dyskineslas and non- motor symptoms. The role of functional imaging in assessing the efficacy of neuroprotective and restorative strategies, is also discussed. it is concluded that, in the future, if technical and cost limitations are adequately addressed, PET imaging may well provide a valuable adjunct to clinical assessment when evaluating the complications and management of PD.
Abstract.
Politis M, Piccini P, Pavese N, Koh S-B, Brooks DJ (2008). Evidence of dopamine dysfunction in the hypothalamus of patients with Parkinson's disease: an <i>in vivo</i> <SUP>11</SUP>C-raclopride PET study.
EXPERIMENTAL NEUROLOGY,
214(1), 112-116.
Author URL.
Politis M, Pavese N, Tai YF, Tabrizi SJ, Barker RA, Piccini P (2008). Hypothalamic involvement in Huntingtons disease: an <i>in vivo</i> PET study.
BRAIN,
131, 2860-2869.
Author URL.
Politis M, Pilinis C, Lekkas TD (2008). ULTRAFINE PARTICLES (UFP) AND HEALTH EFFECTS. DANGEROUS. LIKE NO OTHER PM? REVIEW AND ANALYSIS.
GLOBAL NEST JOURNAL,
10(3), 439-452.
Author URL.
Chapters
de Natale ER, Wilson H, Politis M (2023). Chapter 1 Parkinson's disease and related disorders the pursuit for reliable readouts and the role of neuroimaging. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 3-19.
Tondo G, Comi C, Naldi A, de Natale ER, Politis M (2023). Chapter 12 Neuroimaging in multiple system atrophy. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 311-354.
de Natale ER, Wilson H, Politis M, Niccolini F (2023). Chapter 13 Neuroimaging in progressive supranuclear palsy. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 355-397.
Wilson H, de Natale ER, Politis M, Niccolini F (2023). Chapter 14 Neuroimaging in corticobasal syndrome. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 399-417.
de Natale ER, Wilson H, Niccolini F, Politis M (2023). Chapter 15 Molecular imaging in Huntington's disease. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 421-448.
Belogianni C, Wilson H, de Natale ER, Politis M (2023). Chapter 16 Magnetic resonance imaging in Huntington's disease. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 449-489.
Terry A, de Natale ER, Politis M (2023). Chapter 17 Neuroimaging in essential tremor. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 491-518.
de Natale ER, Wilson H, Udeh-Momoh C, Ford JK, Politis M, Middleton LT (2023). Chapter 18 How molecular imaging studies can disentangle disease mechanisms in age-related neurodegenerative disorders. In (Ed) Aging, Elsevier, 455-492.
de Natale ER, Wilson H, Politis M (2023). Chapter 18 Neuroimaging of restless legs syndrome. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 519-540.
Terry A, de Natale Rosario E, Politis M (2023). Chapter 19 Neuroimaging in dystonia. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 541-566.
Wilson H, de Natale ER, Politis M (2023). Chapter 2 Advances in magnetic resonance imaging. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 21-52.
Wilson H, Politis M (2023). Chapter 3 Advances in molecular neuroimaging methodology. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 53-66.
de Natale ER, Wilson H, Politis M (2023). Chapter 4 Dopaminergic molecular imaging in familial and idiopathic Parkinson's disease. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 69-104.
Wilson H, Terry A, Politis M (2023). Chapter 6 Molecular imaging beyond dopamine and serotonin in familial and idiopathic Parkinson’s disease. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 121-150.
Verghese JP, de Natale ER, Politis M (2023). Chapter 7 Structural MRI in familial and idiopathic PD. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 151-199.
Verghese JP, de Natale ER, Politis M (2023). Chapter 8 Functional MRI in familial and idiopathic PD. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 201-250.
de Natale ER, Verghese JP, Wilson H, Politis M (2023). Chapter 9 Molecular imaging in prodromal Parkinson’s disease. In (Ed) Neuroimaging in Parkinson�s Disease and Related Disorders, Elsevier, 251-272.
De Natale ER, Wilson H, Politis M (2021). Imaging BiomarkersBiomarkers in Huntington’s DiseaseHuntington’s disease (HD). In (Ed) Neurodegenerative Diseases Biomarkers, Springer Nature, 457-505.
Wilson H, de Natale ER, Politis M (2021). Nucleus basalis of Meynert degeneration predicts cognitive impairment in Parkinson's disease. In (Ed)
Handbook of Clinical Neurology, 189-205.
Abstract:
Nucleus basalis of Meynert degeneration predicts cognitive impairment in Parkinson's disease
Abstract.
de Natale ER, Wilson H, Politis M (2021). Serotonergic imaging in Parkinson's disease. In (Ed)
Progress in Brain Research, 303-338.
Abstract:
Serotonergic imaging in Parkinson's disease
Abstract.
Tondo G, Esposito M, Dervenoulas G, Wilson H, Politis M, Pagano G (2019). Hybrid PET-MRI Applications in Movement Disorders. In (Ed)
International Review of Neurobiology, 211-257.
Abstract:
Hybrid PET-MRI Applications in Movement Disorders
Abstract.
Cousins O, Yousaf T, Wilson H, Pagano G, Politis M (2019). Molecular Imaging of Dementia with Lewy Bodies. In (Ed)
International Review of Neurobiology, 59-93.
Abstract:
Molecular Imaging of Dementia with Lewy Bodies
Abstract.
Yousaf T, Dervenoulas G, Politis M (2018). Advances in MRI Methodology. In (Ed)
IMAGING IN MOVEMENT DISORDERS: IMAGING METHODOLOGY AND APPLICATIONS IN PARKINSON'S DISEASE, 31-76.
Author URL.
de Natale ER, Wilson H, Pagano G, Politis M (2018). Imaging Transplantation in Movement Disorders. In (Ed)
IMAGING IN MOVEMENT DISORDERS: IMAGING APPLICATIONS IN NON-PARKINSONIAN AND OTHER MOVEMENT DISORDERS, 213-263.
Author URL.
Politis M (2018). Imaging in Movement Disorders: Imaging Applications in NonParkinsonian and Other Movement Disorders PREFACE. In (Ed)
IMAGING IN MOVEMENT DISORDERS: IMAGING APPLICATIONS IN NON-PARKINSONIAN AND OTHER MOVEMENT DISORDERS, IX-X.
Author URL.
Politis M (2018). Imaging in Movement Disorders: Imaging Methodology and Applications in Parkinson's Disease PREFACE. In (Ed)
IMAGING IN MOVEMENT DISORDERS: IMAGING METHODOLOGY AND APPLICATIONS IN PARKINSON'S DISEASE, XV-XVI.
Author URL.
Politis M (2018). Imaging in Movement Disorders: Imaging in Atypical Parkinsonism and Familial Movement Disorders PREFACE. In (Ed)
IMAGING IN MOVEMENT DISORDERS: IMAGING IN ATYPICAL PARKINSONISM AND FAMILIAL MOVEMENT DISORDERS, XI-XII.
Author URL.
Wilson H, Politis M (2018). Molecular Imaging in Huntington's Disease. In (Ed)
IMAGING IN MOVEMENT DISORDERS: IMAGING IN ATYPICAL PARKINSONISM AND FAMILIAL MOVEMENT DISORDERS, 289-333.
Author URL.
de Natale ER, Niccolini F, Wilson H, Politis M (2018). Molecular Imaging of the Dopaminergic System in Idiopathic Parkinson's Disease. In (Ed)
IMAGING IN MOVEMENT DISORDERS: IMAGING METHODOLOGY AND APPLICATIONS IN PARKINSON'S DISEASE, 131-172.
Author URL.
Pagano G, Politis M (2018). Molecular Imaging of the Serotonergic System in Parkinson's Disease. In (Ed)
IMAGING IN MOVEMENT DISORDERS: IMAGING METHODOLOGY AND APPLICATIONS IN PARKINSON'S DISEASE, 173-210.
Author URL.
Wilson H, Dervenoulas G, Politis M (2018). Structural Magnetic Resonance Imaging in Huntington's Disease. In (Ed)
IMAGING IN MOVEMENT DISORDERS: IMAGING IN ATYPICAL PARKINSONISM AND FAMILIAL MOVEMENT DISORDERS, 335-380.
Author URL.
Politis M, Pagano G, Niccolini F (2017). Imaging in Parkinson's Disease. In (Ed)
PARKINSON'S DISEASE, 233-274.
Author URL.
Yousaf T, Wilson H, Politis M (2017). Imaging the Nonmotor Symptoms in Parkinson's Disease. In (Ed)
NONMOTOR PARKINSON'S: THE HIDDEN FACE: THE MANY HIDDEN FACES, 179-257.
Author URL.
Politis M, Piccini P (2012). <i>In vivo</i> imaging of the integration and function of nigral grafts in clinical trials. In (Ed)
FUNCTIONAL NEURAL TRANSPLANTATION III PRIMARY AND STEM CELL THERAPIES FOR BRAIN REPAIR, PT I, 199-220.
Author URL.
Su P, Politis M (2012). The role of microglia in neurodegenerative disease. In (Ed)
Microglia: Biology, Functions and Roles in Disease, 93-117.
Abstract:
The role of microglia in neurodegenerative disease
Abstract.
Piccini P, Politis M (2011). Cell-Based Therapies. In (Ed)
Imaging in Parkinson's Disease.
Abstract:
Cell-Based Therapies
Abstract.
Politis M, Loane C (2011). Imaging Dyskinesias in Parkinson’s Disease. In (Ed) Diagnosis and Treatment of Parkinson's Disease, IntechOpen.
Conferences
van Wamelen D, Politis M, Aarsland D, Odin P, van Laar T, Henriksen T, Corcoran B, Vivian G, Wilson H, Parry M, et al (2019). APOmorphine infusion and aMYLoid deposition in Parkinson's disease (APOMYL): preliminary clinical and amyloid imaging data.
Author URL.
van Wamelen D, Politis M, Aarsland D, Odin P, van Laar T, Henriksen T, Corcoran B, Vivian G, Parry M, Mulholland N, et al (2019). APOmorphine infusion and aMYLoid deposition in Parkinson's disease (APOMYL): preliminary clinical and amyloid imaging data.
Author URL.
Chandra A, Farrell C, Wilson H, Dervenoulas G, De Natale E, Politis M (2019). Aquaporin-4 genetic variation is associated with disease stage progression and pathology in patients with Alzheimer's disease.
Author URL.
Caminiti SP, Pagano G, Dervenoulas G, Yousaf T, Wilson H, Politis M (2019). Arterial spin labelling detects striatal hypoperfusion in early drug-naive patients with Parkinson's disease.
Author URL.
Caminiti SP, Pagano G, Dervenoulas G, Yousaf T, Wilson H, Politis M (2019). Arterial spin labelling detects subcortical hypoperfusion in early drug-naive patients with Parkinson's disease.
Author URL.
Yousaf T, Pagano G, Wilson H, Corcoran B, Vivian G, Politis M (2019). Comparison between [11C]PE2I PET and [123I]FP-CIT SPECT as markers of DAT expression in early Parkinson's disease.
Author URL.
Pagano G, Wilson H, Yousaf T, Niccolini F, Khan N, Martino D, Gunn R, Rabiner E, Piccini P, Foltynie T, et al (2019). Comparison of PDE10A and DAT expression as markers of disease burden in early Parkinson's disease.
Author URL.
Pagano G, Wilson H, Yousaf T, Niccolini F, Khan N, Martino D, Gunn R, Rabiner E, Piccini P, Foltynie T, et al (2019). Comparison of PDE10A and DAT expression as markers of disease burden in early Parkinson's disease.
Author URL.
De Natale ER, Caminiti SP, Chappell Z, Yousaf T, Wilson H, Politis M (2019). Connectivity alterations in dopaminergic and cholinergic networks mediate cognitive performance in patients with Parkinson's disease: a resting-state fMRI study.
Author URL.
de Natale ER, Caminiti SP, Chappell Z, Yousaf T, Wilson H, Politis M (2019). Connectivity alterations in dopaminergic and cholinergic networks mediate cognitive performance in patients with Parkinson's disease: a resting-state fMRI study.
Author URL.
Farrell C, Pagano G, De Natale E, Politis M (2019). Depressive Symptoms are Associated with Lower Locus Coeruleus Volumes in Parkinson's disease.
Author URL.
Farrell C, Pagano G, de Natale E, Politis M (2019). Depressive symptoms are associated with lower locus coeruleus volumes in Parkinson's disease.
Author URL.
Carotenuto A, Giordano B, Dervenoulas G, Wilson H, Veronese M, Chappell Z, Polychronis S, Mackewn J, Turkheimer F, Williams SC, et al (2019). Direct comparison between T1/T2-weighted ratio MRI and [18F] florbetaben PET imaging as measures of myelin integrity in multiple sclerosis.
Author URL.
Contreras VS, Tayyabah Y, Caminiti S, Politis M (2019). Drooling in Parkinson's Disease: a [123I]FP-CIT SPECT study.
Author URL.
Contreras VCS, Tayyabah Y, Caminiti S, Politis M (2019). Drooling in Parkinson's disease: an [123I] FP-CIT SPECT study.
Author URL.
Schubert JJ, Veronese M, Bodini B, Tonietto M, Stankoff B, Martin-Bastida A, Politis M, Piccini P, Turkheimer FE (2019). Dynamic PET with 11C-and 18F-tracers for measuring cerebrospinal fluid alterations in multiple sclerosis.
Author URL.
Wilson H, Niccolini F, Dervenoulas G, Tyacke R, Myers J, Gunn R, Nutt D, Rabiner E, Tabrizi S, Politis M, et al (2019). Evaluation of Imidazoline 2 binding sites reflecting astroglia pathology in Huntington's Disease: an in vivo [11C]BU99008 PET study.
Author URL.
Wilson H, Dervenoulas G, Pagano G, Tyacke R, Myers J, Gunn R, Rabiner E, Nutt D, Politis M (2019). Evaluation of Imidazoline 2 binding sites reflecting astroglia pathology in Parkinson's Disease: an in vivo [11C]BU99008 PET study.
Author URL.
Wilson H, Dervenoulas G, Pagano G, Tyacke R, Myers J, Gunn R, Rabiner E, Nutt DJ, Politis M (2019). Evaluation of Imidazoline 2 binding sites reflecting astroglia pathology in Parkinson's disease: an in vivo [11C] BU99008 PET study.
Author URL.
Wilson H, Niccolini F, Dervenoulas G, Tyacke R, Myers J, Gunn R, Nutt DJ, Rabiner E, Tabrizi SJ, Politis M, et al (2019). Evaluation of imidazoline 2 binding sites reflecting astroglia pathology in Huntington's disease: an in vivo [11C] BU99008 PET study.
Author URL.
Caminiti SP, Chappell Z, Carotenuto A, Dervenoulas G, Yousaf T, Pagano G, Wilson H, Politis M (2019). Evidence of altered Serotonergic Network in Parkinson's disease by using a multi-modal MRI and PET imaging approach.
Author URL.
Caminiti SP, Chappell Z, Carotenuto A, Dervenoulas G, Yousaf T, Pagano G, Wilson H, Politis M (2019). Evidence of altered Serotonergic Network in Parkinson's disease by using a multimodal MRI and PET imaging approach.
Author URL.
Yousaf T, Dervenoulas G, Pagano G, Loane C, Wilson H, Chandra A, Cousins O, Gunn R, Rabiner E, Niccolini F, et al (2019). Functional connectivity and microstructural alterations in regions of synaptic density loss in DLB and PDD.
Author URL.
Yousaf T, Dervenoulos G, Pagano G, Loane C, Wilson H, Chandra A, Cousins O, Gunn R, Rabiner E, Niccolini F, et al (2019). Functional connectivity and microstructural alterations in regions of synaptic density loss in DLB and PDD.
Author URL.
Contreras VS, Tayyabah Y, Caminiti S, Politis M (2019). Gait impairment in Parkinson's Disease: an [123I]FP-CIT SPECT study.
Author URL.
Contreras VCS, Tayyabah Y, Caminiti SP, Politis M (2019). Gait impairment in Parkinson's disease: an [123I]FP-CIT SPECT study.
Author URL.
Chandra A, Pagano G, Yousaf T, Wilson H, Politis M (2019). Imaging Parkinson's disease pathology: a comparison between neuromelanin-sensitive MRI, susceptibility weighted imaging and [11C]PE2I DAT PET.
Author URL.
Carotenuto A, Wilson H, Giordano B, Caminiti S, Chappell Z, Dervenoulas G, Williams SC, Hammers A, Silber E, Brex PA, et al (2019). Impairment of neurotransmitter networks in patients with Multiple Sclerosis: Clinical implications.
Author URL.
Carotenuto A, Wilson H, Giordano B, Chappell Z, Dervenoulas G, Williams SC, Hammers A, Silber E, Brex PA, Politis M, et al (2019). In vivo evaluation of Multiple Sclerosis pathology with combined perfusion and diffusion MR imaging.
Author URL.
Rota S, Yousaf T, Wilson H, Dervenoulas G, Pagano G, Aarsland D, Politis M (2019). In vivo increased striatal iron deposition in Parkinson's Disease Dementia and Dementia with Lewy Body.
Author URL.
Rota S, Yousaf T, Wilson H, Dervenoulas G, Pagano G, Aarsland D, Politis M (2019). In vivo increased striatal iron deposition in Parkinson's disease dementia and dementia with Lewy body.
Author URL.
Chandra A, Farrell C, Wilson H, De Natale E, Politis M (2019). LRP1 genetic variation is associated with disease stage progression and pathology in patients with Alzheimer's disease.
Author URL.
Chappell Z, Yousaf T, Wilson H, Politis M (2019). Longitudinal Microstructural Changes in Mild Cognitive Impairment.
Author URL.
Esposito M, Yousaf T, Wilson H, Peluso S, Santoro L, Manganelli F, Pagano G, Politis M (2019). Microstructural Changes in Basal Ganglia and Cerebellar Networks in Patients with Idiopathic Blepharospasm.
Author URL.
Pagano G, Wilson H, Mansur A, Caminiti S, Comley R, Tsukada H, Gunn R, Rabiner E, Politis M (2019). Mitochondrial Complex 1, Sigma 1 Receptor and Synaptic Vesicle protein 2A density in early de novo patients with Parkinson's Disease: pilot PET data.
Author URL.
Pagano G, Wilson H, Mansur A, Caminiti SP, Comley R, Tsukada H, Gunn R, Rabiner E, Politis M (2019). Mitochondrial complex 1, sigma 1 receptor and synaptic vesicle protein 2A density in early de novo patients with Parkinson's disease: pilot PET data.
Author URL.
Chappell Z, Wilson H, Politis M (2019). Motor Networks in Tremor-Dominant Parkinson's Disease. A resting-state functional MRI and diffusion tensor imaging analysis.
Author URL.
Cousins O, Wilson H, Yousaf T, Caminiti S, Politis M (2019). Neuroanatomical and clinical predictors of pain in patients with early de novo Parkinson's disease.
Author URL.
Cousins O, Wilson H, Yousaf T, Caminiti SP, Politis M (2019). Neuroanatomical and clinical predictors of pain in patients with early de novo Parkinson's disease.
Author URL.
Cousins O, Pagano G, Belogianni C, Politis M (2019). Neuroanatomical changes in hypertensive patients may underlie increased risk of cognitive impairment.
Author URL.
de Natale ER, Wilson H, Dervenoulas G, Niccolini F, Tabrizi SJ, Politis M (2019). Neuromelanin MRI detects monoaminergic cell loss in Huntington Disease Expansion Gene Carriers.
Author URL.
De Natale ER, Wilson H, Dervenoulas G, Niccolini F, Tabrizi SJ, Politis M (2019). Neuromelanin MRI detects monoaminergic cell loss in Huntington disease expansion gene carriers.
Author URL.
Polychronis S, Pagano G, Contreras VCS, Yousaf T, Politis M (2019). Neuronal Network Underlying Dysphagia in Parkinson's Disease.
Author URL.
Polychronis S, Pagano G, Contreras VCS, Yousaf T, Politis M (2019). Neuronal Network Underlying Speech Difficulties in Parkinson's Disease.
Author URL.
Polychronis S, Pagano G, Contreras VCS, Yousaf T, Politis M (2019). Neuronal networks underlying dysphagia in Parkinson's disease.
Author URL.
Polychronis S, Pagano G, Contreras VCS, Yousaf T, Politis M (2019). Neuronal networks underlying speech difficulties in Parkinson's disease.
Author URL.
Chappell Z, Pagano G, Wilson H, Niccolini F, Gunn R, Rabiner E, Foltynie T, Politis M (2019). Phosphodiesterase 10A and cognition in Parkinson's disease.
Author URL.
Chappell Z, Pagano G, Wilson H, Niccolini F, Gunn R, Rabiner E, Foltynie T, Politis M (2019). Phosphodiesterase 10A and cognition in Parkinson's disease.
Author URL.
Tagliente S, Wilson H, Chappell Z, Yousaf T, De Natale E, Pagano G, Politis M (2019). Probabilistic tractography study of the nigrostriatal pathway in Parkinson's disease.
Author URL.
de Natale ER, Wilson H, Dervenoulas G, Niccolini F, Tabrizi SJ, Politis M (2019). Quantification of regional iron content with Susceptibility Weighted Imaging in Huntington Disease Expansion Gene Carriers.
Author URL.
De Natale ER, Wilson H, Dervenoulas G, Niccolini F, Tabrizi SJ, Politis M (2019). Quantification of regional iron content with susceptibility weighted imaging in huntington disease expansion gene carriers.
Author URL.
Cousins O, Pagano G, Schulz J, Dervenoulas G, Wilson H, Caminiti S, Polychronis S, Politis M (2019). Semantic fluency impairment and amygdala atrophy are predictive factors for the development of Parkinson's disease dementia.
Author URL.
Cousins O, Pagano G, Schulz J, Dervenoulas G, Wilson H, Caminiti SP, Polychronis S, Politis M (2019). Semantic fluency impairment and amygdala atrophy are predictive factors for the development of Parkinson's disease dementia.
Author URL.
Yousaf T, Kershaw M, Contreras VS, Vickers P, Pagano G, Politis M (2019). Structural changes in non-manifesting GBA mutation carriers and GBA mutation carriers with Parkinson's disease.
Author URL.
Yousaf T, Kershaw M, Contreras VCS, Pagano G, Vickers P, Politis M (2019). Structural changes in non-manifesting GBA mutation carriers and GBA mutation carriers with Parkinson's disease.
Author URL.
Pagano G, Vickers P, Schulz J, Wilson H, Politis M (2019). Structural connectivity changes in G2019S-LRRK2 gene mutation carriers without manifest Parkinson's disease.
Author URL.
Pagano G, Vickers P, Schulz J, Wilson H, Politis M (2019). Structural connectivity changes in G2019S-LRRK2 gene mutation carriers without manifest Parkinson's disease.
Author URL.
Contreras VS, Pagano G, Bonfante JF, Wilson H, Politis M (2019). Structural connectivity changes in prodromal Parkinson's disease patients: a multimodal MRI study.
Author URL.
Contreras VCS, Pagano G, Bonfante JAF, Wilson H, Politis M (2019). Structural connectivity changes in prodromal Parkinson's disease patients: a multimodal MRI study.
Author URL.
Schulz J, Yousaf T, Oshodin J, Politis M (2019). TOMM40 polymorphism is associated with cerebral β-amyloid load and clinical pathology in Alzheimer's disease dementia.
Author URL.
Chandra A, Cousins O, Politis M (2019). The pathophysiological and clinical significance of soluable TREM2 in Mild Cognitive Impairment and Mild Alzheimer's disease.
Author URL.
Acampora R, Chandra A, Farrell C, Wilson H, Dervenoulas G, De Natale E, Politis M (2019). The role of MAPT single nucleotide polymorphisms in the clinical phenotype of Alzheimer's disease.
Author URL.
Wilson H, Dervenoulas G, Pagano G, Chandra A, Niccolini F, Esposito M, Gunn R, Ricciardi L, Rabiner E, Aarsland D, et al (2019). The role of Synaptic vesicle protein 2A (SV2A) in patients with Parkinson's disease dementia and Dementia with Lewy bodies: an in vivo [11C]UCB-J PET study.
Author URL.
Yousaf T, Rajendran L, Politis M (2019). The role of hyperlipidemia in mild cognitive impairment and Alzheimer's disease.
Author URL.
Wilson H, Dervenoulas G, Pagano G, Chandra A, Niccolini F, Esposito M, Gunn R, Ricciardi L, Rabiner E, Aarsland D, et al (2019). The role of synaptic vesicle protein 2A (SV2A) in patients with Parkinson's disease dementia and dementia with Lewy bodies: an in vivo [11C]UCB-J PET study.
Author URL.
Farrell C, Yousaf T, Politis M (2019). Treating Depression in Parkinson's Disease: a Systematic Literature Review.
Author URL.
Carotenuto A, Giordano B, Dervenoulas G, Wilson H, Veronese M, Chappell Z, Polychronis S, Niccolini F, MacKewn J, Turkheimer FE, et al (2018). <i>In vivo</i> assessment of myelin breakdown pattern in multiple sclerosis: a hybrid PET/MR [18F] florbetaben study.
Author URL.
Carotenuto A, Giordano B, Dervenoulas G, Wilson H, Veronese M, Chappell Z, Polychronis S, Pagano G, MacKewn J, Turkheimer FE, et al (2018). A hybrid [<SUP>18</SUP>F]florbetapir-PET/MR imaging study to assess <i>in vivo</i> demyelination in multiple sclerosis.
Author URL.
Carotenuto A, Wilson H, Giordano B, Chappell Z, Dervenoulas G, Williams SCR, Hammers A, Silber E, Brex PA, Politis M, et al (2018). In vivo evaluation of multiple sclerosis pathology with combined perfusion and diffusion MR imaging.
Author URL.
Li W, Lao-Kaim N, Roussakis A, Martin-Bastida A, Valle-Guzman N, Loane C, Kefalopoulou Z, Politis M, Foltynie T, Barker R, et al (2017). 11C-PE2I and 18F-DOPA PET imaging for assessing the severity and rate of progression in Parkinson's disease: the longitudinal study.
Author URL.
Pagano G, Niccolini F, Wilson H, Yousaf T, Khan N, Martino D, Gunn R, Rabiner E, Politis M (2017). Altered PDE10A expression detectable early in untreated Parkinson's disease patients.
Author URL.
Pagano G, Niccolini F, Wilson H, Yousaf T, Khan N, Martino D, Gunn R, Rabiner E, Politis M (2017). Altered Pde10a Expression Detectable Early in Untreated Parkinson's Disease Patients.
Author URL.
Bastida AM, Lao-Kaim NP, Xing Y, Loane C, Roussakis A, Schwarz ST, Li X, Valle-Guzman N, Mahlknecht P, Paul-Visse G, et al (2017). Assessing longitudinal iron deposition in deep grey matter nuclei with high-pass filtered phase MR Imaging in Parkinson's disease.
Author URL.
Noyce A, Dickson J, Bestwick J, Isaias I, Politis M, Giovannoni G, Warner T, Lees A, Schrag A (2017). Associations of DAT SPECT and TCS with prodromal features of Parkinson's disease: Results in PREDICT-PD participants.
Author URL.
Niccolini F, Diamantopoulos K, Kiosses S, Politis M (2017). Be vigilant for dementia in Parkinson's disease.
Pagano G, Polychronis S, Wilson H, Niccolini F, Politis M (2017). Diabetes mellitus and Parkinson's disease.
Author URL.
Pagano G, Polychronis S, Wilson H, Niccolini F, Politis M (2017). Diabetes mellitus and Parkinson's disease.
Author URL.
Martin-Bastida A, Lao-Kaim N, Xing Y, Loane C, Roussakis A, Schwarz S, Valle-Guzman N, Mahlknecht P, Li X, Paul-Visse G, et al (2017). High-Pass Filtered Phase Mr Imaging to Detect Longitudinal Motor Associations of Iron Accumulation in Parkinson's Disease.
Author URL.
Giordano B, Pagano G, Hood J, Ferrara N, Politis M (2017). Hypertension and Parkinson's disease.
Author URL.
Giordano B, Pagano G, Hood J, Ferrara N, Politis M (2017). Hypertension and Parkinson's disease.
Author URL.
Dervenoulas G, Pagano G, Niccolini F, Giordano B, Politis M (2017). Hypertension linked to Alzheimer's pathology.
Author URL.
Dervenoulas G, Pagano G, Niccolini F, Politis M (2017). IGF-1 levels are associated with CSF pathology and executive dysfunction in de novo Parkinson's disease patients.
Author URL.
Dervenoulas G, Pagano G, Niccolini F, Politis M (2017). IGF-1 levels are associated with CSF pathology and executive dysfunction in de novo Parkinson's disease patients.
Author URL.
Niccolini F, Wilson H, Hirschbichler S, Pagano G, Erro R, Yousaf T, Whittington A, Holton J, Martino D, Rabiner E, et al (2017). In vivo evaluation of tau and amyloid pathology in Corticobasal Syndrome.
Author URL.
Wilson H, Niccolini F, Hirschbichler S, Pagano G, Erro R, Yousaf T, Whittington A, Gunn R, Rabiner E, Bhatia K, et al (2017). In vivo tau and amyloid pathology in Corticobasal Degeneration (CBD).
Author URL.
Niccolini F, Wilson H, Hirschbichler S, Pagano G, Erro R, Yousaf T, Whittington A, Holton J, Martino D, Rabiner E, et al (2017). In-vivo evaluation of tau and amyloid pathology in Corticobasal Syndrome.
Author URL.
Li W, Lao-Kaim N, Roussakis A-A, Martin-Bastida A, Loane C, Valle-Guzman N, Kefalopoulou Z, Politis M, Foltynie T, Barker R, et al (2017). Longitudinal comparison of 11C-PE2I and 18F-DOPA PET for assessing severity and rate of disease progression in patients with Parkinson's disease.
Author URL.
Li W, Lao-Kaim NP, Roussakis A, Martin-Bastida A, Loane C, Valle-Guzman N, Kefalopoulou Z, Politis M, Foltynie T, Barker RA, et al (2017). Longitudinal comparison of 11C-PE2I and 18F-DOPA pet for assessing severity and rate of disease progression in patients with Parkinson's disease.
Author URL.
Niccolini F, Mencacci NE, Rabiner E, Salpietro V, Pagano G, Balint B, Houlden H, Gunn R, Wood NW, Bhatia KP, et al (2017). Loss of PDE10A expression in patients with PDE10A and ADYC5 mutations.
Author URL.
Niccolini F, Mencacci N, Rabiner E, Salpietro V, Pagano G, Balint B, Houlden H, Gunn R, Wood N, Bhatia K, et al (2017). Loss of PDE10A expression in patients with PDE10A and ADYC5 mutations.
Author URL.
Bonfante JF, Pagano G, Politis M (2017). Neuroimaging studies in familial forms of Parkinson's disease: a systematic review.
Author URL.
Bonfante JAF, Pagano G, Politis M (2017). Neuroimaging studies in familial forms of Parkinson's disease: a systematic review.
Author URL.
Niccolini F, Wilson H, Giordano B, Diamantopoulos K, Pagano G, Chaudhuri KR, Politis M (2017). Non-motor symptom burden is associated with thalamic atrophy in Parkinson's disease.
Author URL.
Niccolini F, Wilson H, Giordano B, Diamantopoulos K, Pagano G, Chaudhuri KR, Politis M (2017). Non-motor symptom burden is associated with thalamic atrophy in Parkinson's disease.
Author URL.
Niccolini F, Wilson H, Giordano B, Diamantopoulos K, Pagano G, Chaudhuri KR, Politis M (2017). Non-motor symptom burden is associated with thalamic atrophy in Parkinson's disease.
Author URL.
Wilson H, Yousaf T, Pagano G, Politis M (2017). Pain and Parkinson's disease.
Author URL.
Wilson H, Yousaf T, Pagano G, Politis M (2017). Pain and Parkinson's disease.
Author URL.
Wilson H, Pagano G, Niccolini F, Muhlert N, Coello C, Tziortzi A, Searle G, Gunn R, Rabiner E, Foltynie T, et al (2017). Phosphodiesterases and striatal pathways in Parkinson's disease.
Author URL.
Wilson H, Pagano G, Niccolini F, Muhlert N, Coello C, Tziortzi A, Searle G, Gunn R, Rabiner E, Foltynie T, et al (2017). Phosphodiesterases and striatal pathways in Parkinson's disease.
Author URL.
Pagano G, Wilson H, Niccolini F, Muhlert N, Coello C, Tziortzi A, Searle G, Gunn R, Rabiner E, Foltynie T, et al (2017). Phosphodiesterases and striatal pathways in Parkinson's disease.
Author URL.
Pagano G, Yousaf T, Loane C, Polychronis S, Wilson H, Giordano B, Niccolini F, Politis M (2017). Predict Cognitive Decline with Clinical Markers in Parkinson's Disease.
Author URL.
Pagano G, Yousaf T, Loane C, Polychronis S, Wilson H, Giordano B, Niccolini F, Politis M (2017). Predict cognitive decline with clinical markers in Parkinson's disease.
Author URL.
Yousaf T, Pagano G, Niccolini F, Politis M (2017). Predict cognitive decline with non-clinical markers in Parkinson's disease.
Author URL.
Yousaf T, Pagano G, Niccolini F, Politis M (2017). Predict cognitive decline with non-clinical markers in Parkinson's disease.
Author URL.
Batash T, Newman H, Barak A, Zayit-Soudry S, Pras E, Banin E, Politis M, Loewenstein A, Neudorfer M (2017). Retinitis pigmentosa-associated cystoid macular edema has inflammatory optical density characteristics.
Author URL.
Roussakis AA, Lao-Kaim N, Martin-Bastida A, Valle-Guzman N, Politis M, Foltynie T, Barker R, Piccini P (2017). Serotonin-to-dopamine transporter ratios in Parkinson's dyskinesias: the longitudinal study.
Author URL.
Polychronis S, Niccolini F, Pagano G, Politis M (2017). Speech difficulties are linked to striatal dopaminergic deficits and cognitive decline in early de novo patients with Parkinson's disease.
Author URL.
Polychronis S, Niccolini F, Pagano G, Politis M (2017). Speech difficulties are linked to striatal dopaminergic deficits and cognitive decline in early de novo patients with Parkinson's disease.
Author URL.
Polychronis S, Dervenoulas G, Pagano G, Niccolini F, Politis M (2017). Swallowing difficulties and Parkinson's disease.
Author URL.
Polychronis S, Dervenoulas G, Pagano G, Niccolini F, Politis M (2017). Swallowing difficulties and Parkinson's disease.
Author URL.
Yousaf T, Pagano G, Niccolini F, Politis M (2017). TOMM40 polymorphism is associated with cognitive and CSF pathology in patients with dementia.
Author URL.
Wilson H, Pagano G, Niccolini F, Muhlert N, Coello C, Mehta M, Searle G, Gunn R, Rabiner E, Foltynie T, et al (2017). The role of phosphodiesterase 4 in sleep disturbances in Parkinson's disease.
Author URL.
Wilson H, Pagano G, Niccolini F, Muhlert N, Coello C, Mehta M, Searle G, Gunn R, Rabiner E, Foltynie T, et al (2017). The role of phosphodiesterase 4 in sleep disturbances in Parkinson's disease.
Author URL.
Yousaf T, Pagano G, Niccolini F, Politis M (2016). Comorbidity and Parkinson's disease phenotype, dopaminergic function and CSF biomarkers.
Author URL.
Li W, Lao-Kaim NP, Roussakis AA, Martin-Bastida A, Loane C, Valle-Guzman N, Kefalopoulou Z, Politis M, Foltynie T, Barker RA, et al (2016). Comparison of DAT and DOPA PET tracer for assessing severity and progression in patients with Parkinson's disease.
Author URL.
Pagano G, Niccolini F, Politis M (2016). Constipation in early de novo Parkinson's disease: Prevalence and correlates with clinical features, imaging and non-imaging biomarkers.
Author URL.
Yousaf T, Pagano G, Niccolini F, Politis M (2016). Excessive daytime sleepiness is mediated by loss of caudate dopaminergic function in Parkinson's disease.
Author URL.
Bastida AM, Lao-Kaim N, Roussakis A-A, Politis M, Li W, Valle-Guzman N, Kefalopoulou Z, Paul G, Widner H, Foltynie T, et al (2016). Imaging nigrostriatal circuitry with 11C-PE2I PET and neuromelanin-sensitive MR in Parkinson's disease.
Author URL.
Roussakis A-A, Lao-Kaim N, Bastida AM, Valle-Guzman N, Kefalopoulou Z, Paul G, Widner H, Politis M, Foltynie T, Barker RA, et al (2016). Increased serotonin-to-dopamine transporter ratios in Parkinson's disease dyskinesias: a longitudinal study.
Author URL.
Roussakis A-A, Lao-Kaim N, Martin-Bastida A, Valle-Guzman N, Kefalopoulou Z, Paul-Visse G, Widner H, Politis M, Foltynie T, Barker R, et al (2016). LEVODOPA-INDUCED DYSKINESIA IN PARKINSON'S: a LONGITUDINAL PET STUDY.
Author URL.
Wilson H, Niccolini F, Haider S, Marques TR, Pagano G, Coello C, Natesan S, Kapur S, Rabiner EA, Gunn RN, et al (2016). Loss of extra-striatal phosphodiesterase 10A expression in early premanifest Huntington's disease gene carriers.
Author URL.
Martin-Bastida A, Lao-Kaim NP, Roussakis AA, Li W, Politis M, Valle-Guzman N, Kefalopoulou Z, Paul G, Widner H, Foltynie T, et al (2016). Multimodal imaging assessment of nigrostriatal pathway in Parkinson's disease using 11C-PE2I PET and neuromelanin-sensitive MR.
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Wilson H, Niccolini F, Pellicano C, Piccini P, Politis M (2016). Staging and clinical correlates of cortical thinning in Parkinson's disease.
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Niccolini F, Pagano G, Fusar-Poli P, Wood A, Mrzljak L, Sampaio C, Politis M (2016). Striatal molecular alterations in Huntington's disease gene expansion carriers: a systematic review and meta-analysis of PET studies.
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Polychronis S, Pagano G, Politis M (2016). The role of diabetes mellitus and hyperglycemia in early de novo Parkinson's disease patients.
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Polychronis S, Pagano G, Politis M (2016). The role of striatal dopaminergic terminals in early de novo PD patients with speech impairment.
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Pagano G, Niccolini F, Politis M (2016). α-synuclein CSF levels correlate with urinary dysfunction in early de novo Parkinson's disease patients.
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Sauerbier A, Martinez-Martin P, Politis M, Rizos A, Troja N, Mulholland N, Vivian G, Cocoran B, Trivedi D, Perkins L, et al (2015). Dopamine transporter scan (DaTscan) and clinical global impression of severity of Parkinson's disease: Data from a non motor natural history study.
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Perkins L, Politis M, Niccolini F, Sauerbier A, Inniss R, Martin A, Trivedi D, Ray-Chaudhuri K (2015). Effect of acute non-oral dopaminergic (apomorphine and levodopa) treatment on non-motor symptoms in Parkinson's disease.
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Roussakis A-A, Politis M, Towey D, Piccini P (2015). Levodopa induced dyskinesias: increased serotonin to dopamine transporter ratios in the putamen of Parkinson's disease patients.
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Niccolini F, Foltynie T, Marques TR, Searle G, Natesan S, Kapur S, Rabiner E, Gunn R, Piccini P, Politis M, et al (2015). Loss of phosphodiesterase 10A signalling is associated with progression and severity in patients with Parkinson's disease.
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Bastida AM, Politis M, Loane C, Lao-Kaim N, Valle-Guzman N, Kefalopoulou Z, Paul G, Widner H, Foltynie T, Barker R, et al (2015). Nigral iron susceptibility in Parkinson's disease (PD).
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Roussakis A-A, Politis M, Towey D, Piccini P (2015). SEROTONIN-TO-DOPAMINE TRANSPORTER RATIOS IN THE STRIATUM OF PATIENTS WITH PARKINSON'S DISEASE: IMPACT ON LEVODOPA-INDUCED DYSKINESIAS.
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Martin-Bastida A, Politis M, Loane C, Lao-Kaim N, Valle-Guzman N, Kefalopoulou Z, Gesine P, Foltynie T, Barker R, Piccini P, et al (2015). SUSCEPTIBILITY WEIGHTED IMAGING TO DETECT NIGRAL IRON ACCUMULATION IN PARKINSON'S DISEASE.
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Marques TR, Natesan S, Niccolini F, Politis M, Gunn R, Searle G, Howes O, Rabiner E, Kapur S (2015). The role of Phosphodiesterase 10A in Schizophrenia: a Positron Emission Tomography study using [<SUP>11</SUP>C]IMA107.
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Niccolini F, Marques TR, Haider S, Searle G, Natesan S, Kapur S, Rabiner E, Gunn R, Tabrizi S, Politis M, et al (2014). Brain phosphodiesterase 10A (PDE-10A) density in early premanifest HD gene carriers.
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Niccolini F, Marques TR, Haider S, Muhlert N, Tzortzi AC, Loane C, Searle GE, Robertson N, Natesan S, Piccini P, et al (2014). Brain phosphodiesterase 10A (PDE-10A) density in early premanifest HD gene carriers.
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Niccolini F, Marques TR, Haider S, Muhlert N, Tzortzi AC, Loane C, Searle GE, Robertson N, Natesan S, Piccini P, et al (2014). Brain phosphodiesterase 10A (PDE-10A) density in early premanifest HD gene carriers.
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Wu K, Politis M, O'Sullivan SS, Lawrence AD, Warsi S, Bose S, Lees AJ, Piccini P (2014). Co-morbid impulse control disorders in Parkinson's disease: a positron emission tomography study.
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Wu K, Politis M, O'Sullivan SS, Lawrence AD, Warsi S, Lees A, Piccini P (2014). Problematic internet use in Parkinson's disease.
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Kefalopoulou Z, Politis M, Piccini P, Mencacci N, Bhatia K, Jahanshahi M, Widner H, Rehncrona S, Brundin P, Bjoerklund A, et al (2014). Very long-term clinical outcome of fetal cell transplantation for Parkinson's disease.
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Politis M, Giannetti P, Niccolini F, Su P, Turkheimer F, Waldman A, Reynolds R, Nicholas R, Piccini P (2013). Decreased Microglial Activation Precedes Stabilization of Disability in Multiple Sclerosis Patients Treated with Natalizumab.
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Niccolini F, Giannetti P, Politis M, Su P, Turkheimer F, Waldman A, Reynolds R, Nicholas R, Piccini P (2013). In Vivo Detection of Thalamo-Cortical Pathology in Patients with Clinical Isolated Syndrome.
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Giannetti P, Politis M, Su P, Turkheimer F, Malik O, Keihaninejad S, Waldman A, Niccolini F, Reynolds R, Nicholas R, et al (2013). Microglia Activation in Clinically Isolated Syndrome: 11C11195PK-PET Change within Normal Appearing White Matter and Deep Grey Matter Structures.
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Politis M, Loane C, Pavese N, Brooks D, Chaudhuri K, Piccini P (2013). Sustained and Prolonged Striatal Dopamine Levels in Parkinson's Patients Following Enteral L-Dopa Gel Infusion: an in Vivo 11C-Raclopride PET Study.
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Loane C, Politis M, Wu K, O'Sullivan SS, Woodhead Z, Lawrence AD, Lees AJ, Piccini P (2012). Drug-cue elicited frontal and limbic dysfunction in Parkinson's disease patients with dopamine dysregulation syndrome.
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Wu K, O'Keeffe D, Politis M, O'Keeffe G, Bose S, Brooks DJ, Barker R, Piccini P (2012). IN VIVO EVIDENCE OF COMT VAL158MET FUNCTIONAL POLYMORPHISM MODULATES DIFFERENT LEVELS OF DOPAMINE TURNOVER IN PARKINSON'S DISEASE: AN 18F-DOPA PET STUDY.
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Garvey L, Pavese N, Politis M, Ramlackhansingh A, Taylor-Robinson S, Brooks D, Winston A (2012). Microglial cell activation is visualised with [11C]-PK11195 Positron Emission Tomography (PET) in neuro-asymptomatic HIV infected subjects on effective antiretroviral therapy.
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Politis M, Loane C, Wu K, O'Sullivan S, Woodhead Z, Kiferle L, Lawrence AD, Lees AJ, Piccini P (2012). Neural correlates of hypersexuality in Parkinson's disease.
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Giannetti P, Politis M, Su P, Turkheimer FE, Malik O, Keihaninejad S, Wu K, Reynolds R, Nicholas R, Piccini P, et al (2012). PK11195-PET Enhancement in Black Holes Correlates with Disability and Outcome in Progressive Multiple Sclerosis.
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Politis M, Wu K, Loane C, Kiferle L, Molloy S, Bain P, Brooks D, Piccini P (2012). Serotonergic mediated peak-dose L-DOPA-induced dyskinesias in Parkinson's disease.
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Loane C, Politis M, Wu K, Brooks DJ, Piccini P (2012). Serotonergic presynaptic terminal density in caudate nucleus inversely correlates with severity of action-postural tremor in PD.
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Giannetti P, Politis M, Su P, Turkheimer F, Wu K, Reynolds R, Nicholas R, Piccini P (2011). Two different roles for microglia in vivo in T1 black holes in relapsing and progressive multiple sclerosis?.
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Politis M, Giannetti P, Su P, Turkheimer F, Keihaninejad S, Wu K, Waldman A, Reynolds R, Nicholas R, Piccini P, et al (2010). Cortical Microglial Activation is Associated with Disability in Secondary Progressive Multiple Sclerosis: an <i>In Vivo</i> Imaging Study.
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Wu K, Politis M, O'Sullivan S, Bose S, Lees A, Piccini P (2010). Impulse Control Disorders Subtypes in Parkinson's Disease: Clinical and PET Correlations.
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Wu K, Politis M, Warsi S, Loane C, O'Sullivan S, Lees A, Piccini P (2010). Measuring Severity of Impulse Control Disorders in Parkinson's Disease Using Objective Validated Questionnaire.
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Wu K, O'Sullian S, Politis M, Bose S, Lees A, Piccini P (2010). REWARDING VISUAL CUES INCREASE DOPAMINE NEUROTRANSMISSION IN PARKINSON'S PATIENTS WITH IMPULSE CONTROL DISORDERS: a PET STUDY.
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Politis M, Wu K, Loane C, Kiferle L, Molloy S, Bain P, Brooks DJ, Piccini P (2010). Serotonergic Involvement in L-DOPA-Induced Dyskinesia.
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Politis M, Wu K, Loane C, Kiferle L, Molloy S, Brooks DJ, Piccini P (2010). Serotonergic Terminals Are Differentially Affected in Parkinson's Disease: an <i>In Vivo</i> <SUP>11</SUP>C-DASB PET Study.
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O'Sullivan SS, Politis M, Wu K, Lawrence AD, Evans AH, Bose SK, Lees AJ, Piccini P (2009). Increased dopamine neurotransmission in Parkinson's patients with Impulse control disorders in response to rewarding visual stimuli: a pilot study.
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Politis M, Pavese N, Tai YF, Kiferle L, Brooks DJ, Tabrizi SJ, Barker RA, Piccini P (2009). The limbic-circuitry of Huntington's disease: a combined neuroimaging approach.
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Politis M, Piccini P, Pavese N, Koh S-B, Brooks DJ (2007). Evidence of dopamine dysfunction in the hypothalamus of patients with Parkinson's disease:: an in vivo <SUP>11</SUP>C-raclopride PET study.
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