Overview
Isabel is a Postdoctoral Researcher in the Complex Disease Epigenetics Group where she is investigating the relevance of (epi)genomic changes in neurogenerative conditions such as Alzheimer's disease. She did her PhD under the supervision of Prof Jonathan Mill and Prof Katie Lunnon, which focused on evaluating functional genomics of rodent models relevant for Alzheimer’s Disease. As a postdoctoral researcher she is continuing the work from her PhD.
Qualifications
BSc, MSc, PhD
Career
Isabel Castanho originally graduated in Biomedical Laboratory Sciences at the Polytechnic Institute of Porto, spending part of her final year at the Metropolia University of Applied Sciences in Helsinki.
Isabel took a second degree in Applied Biology at the University of Minho. She also completed a Master’s degree in Health Sciences at the same university, having developed her thesis in the Neuroscience Research Domain of the Life and Health Sciences Research Institute under supervision of Dr Tiago Gil Oliveira. During her Master's degree she investigated the role of lipid signalling pathways in hippocampus functioning.
In 2016 Isabel enrolled in the University of Exeter as a PhD student of the Exeter Doctoral Training Centre (DTC) from the Alzheimer's Society, led by Prof Andrew Randall. As a PhD student, and now as a Postdoc, Isabel has been investigating the relevance of (epi)genomic changes in neurogenerative conditions such as Alzheimer's disease, with a particular interest in changes ocurring with progression of disease.
For more information check her Linkedin profile here.
Publications
Key publications | Publications by category | Publications by year
Publications by category
Journal articles
Marinha LS, Castanho I, Silva RR, Bravo FV, Miranda AM, Xu Y, Point du Jour K, Wenk M, Chan RB, Di Paolo G, et al (In Press). Phospholipase D1 Ablation Disrupts Mouse Longitudinal Hippocampal Axis Organization and Functioning.
Castanho I, Murray TK, Hannon E, Jeffries A, Walker E, Laing E, Baulf H, Harvey J, Bradshaw L, Randall A, et al (2020). Transcriptional Signatures of Tau and Amyloid Neuropathology.
Cell Rep,
30(6), 2040-2054.e5.
Abstract:
Transcriptional Signatures of Tau and Amyloid Neuropathology.
Alzheimer's disease (AD) is associated with the intracellular aggregation of hyperphosphorylated tau and the accumulation of β-amyloid in the neocortex. We use transgenic mice harboring human tau (rTg4510) and amyloid precursor protein (J20) mutations to investigate transcriptional changes associated with the progression of tau and amyloid pathology. rTg4510 mice are characterized by widespread transcriptional differences in the entorhinal cortex with changes paralleling neuropathological burden across multiple brain regions. Differentially expressed transcripts overlap with genes identified in genetic studies of familial and sporadic AD. Systems-level analyses identify discrete co-expression networks associated with the progressive accumulation of tau that are enriched for genes and pathways previously implicated in AD pathology and overlap with co-expression networks identified in human AD cortex. Our data provide further evidence for an immune-response component in the accumulation of tau and reveal molecular pathways associated with the progression of AD neuropathology.
Abstract.
Author URL.
Full text.
Castanho I, Murray T, Hannon E, Jeffries A, Walker E, Laing E, Baulf H, Harvey J, Randall A, Moore K, et al (2019). Transcriptional Signatures of Progressive Neuropathology in Transgenic Models of Tau and Amyloid Pathology.
Publications by year
In Press
Marinha LS, Castanho I, Silva RR, Bravo FV, Miranda AM, Xu Y, Point du Jour K, Wenk M, Chan RB, Di Paolo G, et al (In Press). Phospholipase D1 Ablation Disrupts Mouse Longitudinal Hippocampal Axis Organization and Functioning.
2020
Castanho I, Murray TK, Hannon E, Jeffries A, Walker E, Laing E, Baulf H, Harvey J, Bradshaw L, Randall A, et al (2020). Transcriptional Signatures of Tau and Amyloid Neuropathology.
Cell Rep,
30(6), 2040-2054.e5.
Abstract:
Transcriptional Signatures of Tau and Amyloid Neuropathology.
Alzheimer's disease (AD) is associated with the intracellular aggregation of hyperphosphorylated tau and the accumulation of β-amyloid in the neocortex. We use transgenic mice harboring human tau (rTg4510) and amyloid precursor protein (J20) mutations to investigate transcriptional changes associated with the progression of tau and amyloid pathology. rTg4510 mice are characterized by widespread transcriptional differences in the entorhinal cortex with changes paralleling neuropathological burden across multiple brain regions. Differentially expressed transcripts overlap with genes identified in genetic studies of familial and sporadic AD. Systems-level analyses identify discrete co-expression networks associated with the progressive accumulation of tau that are enriched for genes and pathways previously implicated in AD pathology and overlap with co-expression networks identified in human AD cortex. Our data provide further evidence for an immune-response component in the accumulation of tau and reveal molecular pathways associated with the progression of AD neuropathology.
Abstract.
Author URL.
Full text.
2019
Castanho I, Murray T, Hannon E, Jeffries A, Walker E, Laing E, Baulf H, Harvey J, Randall A, Moore K, et al (2019). Transcriptional Signatures of Progressive Neuropathology in Transgenic Models of Tau and Amyloid Pathology.
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