Lieu: Brunoy.

Abstract: Genome-wide association studies (GWAS) over the last few years have identified genetic risk variants for neurodegenerative diseases Including Alzheimer’s disease. >90% of variants associated with sporadic alzheimer’s disease are located in non-coding regions of the genome and are presumed to affect transcription of nearby genes. In my work, I have developed tools for programmable manipulation of epigenetic states, transcription, and RNA splicing to functionally investigate the mechanism of these genetic variants in neurodegeneration. Using these tools, I aim to understand how major brain cell types – neurons, astrocytes and microglia – differentially contribute to altered cellular signaling pathways both in human neurodegeneration as well as in the neurodegenerative phenotype of the mouse lemur.