Julia TCW

Much of our research focuses on the effects of AD genetic risks, especially Apolipoprotein E4 (APOE4), the most significant risk factor for late-onset AD on human brain cell types. Our lab uses the forward genetic, unbiased multi-Omics computational (bioinformatics) approach to uncover pathways and network defects of AD genetic risks and demonstrate molecular mechanisms of the risk factors in CNS cell types derived from CRISPR/Cas9 genome-edited isogenic and population iPSCs. We develop novel computational pipelines to identify molecular and network drivers and integrate genetics and transcriptomics/proteomics for a functional genomic study. In vitro and in vivo work have been focused on efferocytosis, lipid metabolism, matrisome and inflammation in pure human microglia, astrocytes and organoids (multiple brain cell types as a whole) associated with AD genetic risks. Further, our lab is also collaborating with the industry to find a drug target for AD therapeutics.

We have developed multiple novel CNS cell type protocols including astrocytes, microglia, pericytes, neural progenitors and glutamatergic neurons and continuously put our effort to advance the 2D models to 3D human brain model to establish efficient platforms for drug screen.