Overview
My career in research and specific interest in neuroscience began at The University of Dundee while investigating the role environments play in relapse during morphine addiction under the supervision of Dr Steven Martin. During my study I was also fortunate enough to be awarded a research placement at the University of Strathclyde looking into the role of MKP-2 in cellular apoptosis with Professor Robin Plevin.
After completion of my degree at Dundee I wanted enhance my research skills in Neuroscience. I began an MSc by research in Integrative Neuroscience at the University of Edinburgh with Dr Szu-Han Wang, for which I was awarded The University of Edinburgh UK/EU Master's Scholarship. My research was to identify the behavioural events that can contribute to contextual fear generalisation, an animal model used to mirror a symptom found in PTSD, and their receptor mechanisms.
Since then I have relocated to Exeter University to undertake my PhD under the supervision of Dr Michael Craig.
Qualifications
2015 BSc (First Class Hons) Biomedical Sciences, University of Dundee
2016 MSc Integrative Neuroscience, University of Edinburgh
Research
Research interests
My central interest is to understand the role different brain cells play in generating certain activity patterns and their contribution to health and disease. Specifically, my project is looking to decipher the role interneurons play in the disruption of slow wave oscillations that can be seen in Alzheimer’s disease. It is important to understand the cellular and circuit mechanisms that contribute to the pathophysiology of neurodegenerative diseases such as Alzheimer’s as this can lead to potential therapeutics and preventative measures.
I work in the lab of Dr Michael Craig, with additional supervisors Professor Andrew Randall and Professor Vincenzo Crunelli (Cardiff University). My PhD is funded by the GW4 MRC DTP studentship.
Publications
Key publications | Publications by category | Publications by year
Publications by year
2021
Brady E (2021). An investigation of medial prefrontal cortex – hippocampal circuit function in a mouse model of familial Alzheimer’s disease.
Abstract:
An investigation of medial prefrontal cortex – hippocampal circuit function in a mouse model of familial Alzheimer’s disease
The communication between the medial prefrontal cortex (mPFC) and hippocampus is crucial for spatial memory, decision making and the long-term consolidation of our memories during sleep. This communication is mediated via the temporal coupling of key neuronal oscillations. Alzheimer’s disease (AD) is a progressive neurodegenerative disorder which affects the electrical activity of the brain, causing disrupted neuronal oscillations and a decline in episodic, spatial and working memory. In the preclinical stages of the disease, sleep disruptions are common and are accompanied by impairments to several of the oscillations responsible for long-term memory consolidation in the mPFC-hippocampal circuit. However, less is known about how the functional interactions of the different neuronal oscillations in this circuit are affected. Additionally, impairments to the oscillations involved in spatial memory and decision making in the mPFC-hippocampal circuit are known to occur in first-generation mouse models of amyloidopathy, yet have been scarcely studied in second-generation models. Therefore, using in vivo electrophysiology, the oscillatory activity of this circuit was studied during sleep and exploratory behaviour in the second-generation APPNL-G-F mouse model of amyloidopathy, to investigate potential dysfunctions.
The neuronal oscillations in the mPFC-hippocampal circuit were studied during natural sleep. In these experiments, impairments to local oscillations in the mPFC and CA1 region of the hippocampus were identified, yet long-range coordination of oscillations between brain regions was unaffected. Additionally, the oscillations recorded in CA1 during spatial memory showed local disruptions. Finally, impairments to the function of inhibitory neurons have been proposed to underlie changes to the oscillatory dynamics of neuronal circuit activity in AD. Therefore, immunohistochemical analysis of interneuron protein markers was performed to complement electrophysiological analyses of mPFC and CA1 circuit function. Collectively, these experiments further our understanding of how the mPFC-hippocampal circuit is affected in AD and provide a basis to study the underlying circuit disruptions.
Abstract.
Full text.
Refresh publications
Teaching
Lab Demonstrator - CSC2006 Foundations in Neuroscience
