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As an interdisciplinary researcher, I have identified human serum amyloid P component (hSAP) as a catalytic glycoprotein in the pathogenesis of Alzheimer’s disease (AD), through to following the cellular fate of aluminium adjuvants in clinically approved human vaccinations. My research now seeks to discover the mechanisms involved in the cellular trafficking of amyloid from the periphery to the brain, with the goal of creating effective vaccine adjuvants using three-dimensional (3D) cellular models of AD. The overall project aim is to assess the ineffectiveness of the normally cytoprotective function of healthy cells to selectively degrade intracellular amyloidogenic species in ageing and AD. The accumulation of the neurotoxic β-amyloid peptide within synaptic mitochondria favours their abnormal fission dynamics and fragmentation that follows synaptic loss in AD. Delineating mitochondrial dynamics that drive the accumulation of intracellular reactive oxygen species and the subsequent initiation of pro-apoptotic cell environments will shed light on the pathogenesis of amyloidosis diseases of which in excess of 30 have been identified to date. These proposed studies have generated considerable interest from external UK research funding councils and demonstrate my commitment to securing an independent career in research.
Research Interests
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Alzheimer's Research & Therapyno. 1 (2021)
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