Alzheimer’s disease (AD) is the most common neurodegenerative disorder and a leading cause of dementia worldwide. Clinically, AD involves a progressive decline in memory and cognition, but biologically it is a complex, heterogeneous condition shaped by interactions between genetic risk, aging, and molecular pathways in the brain. While rare mutations in APP, PSEN1, and PSEN2 cause familial early-onset AD, most cases are late-onset and polygenic, driven by many risk loci with small effects.
In our AD genetics project, we aim to move beyond association signals to identify causal genes, understand disease mechanisms, and accelerate therapeutic discovery. We integrate large-scale genomic datasets with brain-relevant multi-omics, systems biology, and machine-learning approaches.
Importantly, our team also performs its own genome-wide association (GWAS) analyses and whole-genome (WGS) sequencing across multiple Alzheimer’s disease cohorts to identify novel risk loci and refine existing genetic signals.
Our work also examines the shared and distinct genetic background between AD and related neurodegenerative synucleinopathies such as Parkinson’s disease (PD), dementia with Lewy bodies (DLB), REM sleep behavior disorder (RBD), and multiple system atrophy (MSA).