About the Event
The Oskar Fischer Lecture Series, led by The University of Texas at Austin’s Mulva Clinic for the Neurosciences, is a campus-wide series featuring invited scholars working at the vanguard of new ideas on the mechanisms, diagnosis and treatment of dementing illnesses.
This lecture features Beth Stevens, Ph.D., presenting “Redefining Microglia states and function in Alzheimer’s Disease.”
About the Lecture
Emerging genetic studies of late-onset Alzheimer’s Disease implicate the brain’s resident macrophages in the pathogenesis of AD. More than half the risk genes associated with late-onset AD are selectively expressed in microglia and peripheral myeloid cells; yet we know little about the underlying biology or how myeloid cells contribute to AD pathogenesis. Using single-cell RNA sequencing and spatial transcriptomics we identified molecular signatures that can be used to localize and monitor distinct microglia functional states in the human and mouse brain. Our results show that microglia assume diverse functional states in development, aging and injury, including populations corresponding to known microglial functions including proliferation, migration, inflammation, and synaptic phagocytosis. We identified several innate immune pathways by which microglia recognize and prune synapses during development and in models of Alzheimer’s Disease, including the classical complement cascade. Illuminating the mechanisms by which developing synaptic circuits are sculpted is providing important insight into understanding how to protect synapses in Alzheimer’s and other neurodegenerative diseases that could lead to new therapies and biomarkers for early diagnoses.
About the Presenter
Beth Stevens, Ph.D., is an associate professor at Harvard Medical School and Boston Children’s Hospital and a member of the Broad Institute. She is a Howard Hughes Medical Institute investigator and has been elected to the National Academy of Medicine.
Her research is focused on understanding how neural-immune interactions in the brain sculpt synapses during normal development and disease, providing insights into the pathological synapse loss of Alzheimer’s disease, dementia and schizophrenia.