I joined the Wellcome Centre for Mitochondrial Research in 2019 after completing my PhD with Dr Chris Morris in 2017 and completing my first post-doctoral appointment with Professor Johannes Attems in 2018.
My career to date has focused on understanding disease mechanisms in Lewy body diseases, including Parkinson’s disease and dementia with Lewy bodies. I am particularly interested in mediators of cellular vulnerability in Lewy body diseases, with a focus on mitochondrial dysfunction and the role of distinct species of alpha-synuclein. My research primarily employs post-mortem human tissues, augmented by mechanistic studies in human model systems, such as neuronal cell cultures.
I have related interests in the neuropathology of other neurodegenerative conditions that have aetiological overlaps with Lewy body disease, including primary mitochondrial encephalopathies, neurodegeneration with brain iron accumulation (formerly Hallervorden-Spatz disease) and Down’s syndrome.
In 2019 I was awarded an Alzheimer’s Research UK Fellowship to study cellular vulnerability in the neocortex using post-mortem tissue and novel human model systems.
Are Lewy bodies really the enemy in Lewy body disease?
Collaborators: Professor Omar El-Agnaf (Qatar Biomedical Research Institute, Qatar; https://www.hbku.edu.qa/en/qbri/staff/dr-omar-el-agnaf)
Lewy body diseases (LBD) are the second most common neurodegenerative disorder after Alzheimer’s disease and are characterised primarily by movement problems. Cognitive symptoms are common in LBD patients and are associated with particularly poor outcomes, but the causative mechanisms underlying such symptoms remain unknown.
Our current studies are investigating the role of interneurons in driving the cognitive symptoms of LBD. Interneurons coordinate brain rhythms that underlie cognitive faculties such as attention and visual perception, processes known to be altered in LBD. Mitochondrial dysfunction is widely reported in LBD brains and, as interneurons have especially high energy demands, they would be particularly vulnerable to dysfunction in such circumstances.
Our current project will use post-mortem brain tissue and novel human model systems to investigate the role of interneurons in cognitive symptoms in LBD.
Sponsor/funder: Alzheimer’s Research UK