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Dr Dominic Simpson

DPhil (Oxon)

Postdoctoral Researcher

Deciphering how genetic risk for Alzheimer’s disease alters human microglial function, neuroinflammation, and amyloid pathology

Techniques

Advanced microscopy & imaging, Bioinformatics, CRISPR, Genomics, Stem cells / iPSCs, Flow cytometry, Mass spec-based proteomics, Next generation sequencing, Single cell / nucleus transcriptomics, Viral-mediated expression

Biography

Dr Dominic Simpson is a postdoctoral research fellow investigating the role of microglia in Alzheimer’s disease. He completed his DPhil at the University of Oxford, where he studied human stem cell-derived models of neurodegeneration, before joining the UK Dementia Research Institute at University College London and the Francis Crick Institute.


His current research focuses on how genetic risk factors for Alzheimer’s disease alter the behaviour of human microglia, the brain’s resident immune cells. In particular, he studies SORL1, a gene strongly linked to Alzheimer’s disease, to understand how its loss of function affects microglial responses to amyloid pathology, inflammatory signalling, and disease progression.


By combining human stem cell models, advanced imaging, molecular profiling, and human microglia transplantation into mouse models of amyloid disease, his work aims to identify mechanisms that could ultimately be targeted to restore protective immune functions in the brain.

Research interest

My research aims to understand how genetic risk for Alzheimer’s disease changes the behaviour of microglia, the brain’s resident immune cells. I am particularly interested in SORL1, a gene strongly linked to Alzheimer’s disease, and how loss of SORL1 function affects the way human microglia sense, respond to, and process amyloid pathology.


Using human stem cell-derived models and transplantation of human microglia into mouse models of Alzheimer's disease, my work investigates how disease-associated genetic changes alter microglial states, inflammatory signalling, and interactions with amyloid plaques. The broader goal is to uncover mechanisms by which Alzheimer’s risk genes contribute to disease progression, and to identify pathways that could eventually be targeted to restore protective microglial function.