Finding Aberrant Glial and Neuronal Dysfunctions That Promote Neurodegeneration in Alzheimer’s Disease and Related Dementia

Alzheimer’s disease (AD) and Frontotemporal lobar degeneration (FTLD) are two highly related neurodegenerative diseases that share several key clinical, genetic and neuropathological features. The goal of my project is to harness the cutting-edge single cell transcriptomic technology to uncover common transcriptomic signatures that contribute to disease progression in AD and FTLD. Results from this study will provide important insights to disease mechanisms and an enriched resource for the scientific community. Ultimately, these results will help discover new treatments for these devastating diseases.

The goal of my project is to unravel new cellular and molecular mechanisms that promote neurodegeneration in Frontotemporal lobar degeneration and Alzheimer’s disease, two common and devastating neurodegenerative diseases. To do so, I am using single cell transcriptomics, a cutting-edge technology that detects changes in gene expression profiles in individual cells, to identify cell type-specific signatures shared across different brain regions from patients with dementia and Alzheimer’s disease. This innovative strategy allows me to focus on how abnormal activation of astrocytes and microglia, the brain’s innate immune cells, contributes to the neuronal loss observed in neurodegenerative diseases. Since there are significant overlaps in the clinical presentation, genetics and disease mechanisms between dementia and Alzheimer’s disease, my results will have major impacts on our understanding of neurodegeneration in a broad context. Once my study is complete, I hope to have identified new therapeutic targets for Alzheimer’s disease and other dementias.