Research interest
Genome-wide association studies (GWAS) have shown that variants in immune system genes including complement and human leukocyte antigen (HLA) genes that encode major histocompatibility (MHC) proteins drive neurodegeneration in AD. My research is two-fold. One to identify a link between complement AD risk genes and complement indued synapse loss using induced pluripotent stem cells (iPSC) from individuals with either a low or high complement polygenic risk score to determine whether complement genetic makeup alters neuronal function and complement dysregulation. Secondly, to understand the HLA association with AD. My team use HLA typing of higher resolution whole-exome sequencing (WES) data, T-cell receptor sequencing and HLA immunopeptidomics to explore the HLA association with AD from an immune perspective.