Sam is examining the genomics of Alzheimer's disease and how genetic variation can impact the microglial response in neuroinflammation.
Sam is part of the Open Targets network working on the mechanisms of neuroinflammation in neurodegeneration in iPSC derived microglia. He joined the Cellular Operations R&D team as a postdoctoral research fellow in 2020 and is on secondment at the University of Oxford with Dr Sally Cowley of the James Martin Stem Cell Facility and Dr Daniel Ebner of the Target Discovery Institute.
To study neuroinflammation in neurodegeneration he is planning to perform a variety of genome-wide CRISPR screens on iPSC derived microglia. These screens will be related to different microglial functions which play a role in inflammation, including phagocytosis, migration, and cytokine production. Once target genes have been identified Sam will return to Sanger and perform validation experiments on individual knockout lines.
Sam has an interest in molecular biology techniques related to functional validation of genomic risk loci in neurodegenerative and neurodevelopmental disorders. This led to a strong love of CRISPR/Cas9 method development to help link genetic risk to functional consequences in cellular models. Alongside the wet lab he also is a keen computational biologist and has interested in exploring how genetic variation impacts alternative splicing, DNA methylation, and gene expression.