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Tara Tracy, Ph.D.

Tara Tracy, Ph.D.

Investigating Synaptic Dysfunction in Human Neuronal Models of Tauopathy

When

March 2, 2017, 10:00 a.m.

Who

Tara Tracy, Ph.D.

Research Scientist, J. David Gladstone Institutes, Gladstone Institute of Neurological Disease, Department of Neurology,
University of California, San Francisco

Where

Fralin Biomedical Research Institute, R1059
2 Riverside Circle, Roanoke, VA 24016

Tauopathies are neurodegenerative diseases, including Alzheimer’s disease (AD) and frontotemporal lobar degeneration with tau inclusions (FTLD-tau), that are characterized by abnormal tau accumulation in the brain linked to cognitive dysfunction. Synapse loss is well documented at late stages of dementia in tauopathy; however, early pathogenic mechanisms that occur at synapses during cognitive decline are poorly understood. Growing evidence suggests that tau causes toxicity in neurons in AD and FTLD-tau. What tau is doing at synapses and how it triggers pathogenesis is unclear. The focus of Dr. Tracy’s research is the investigation of the mechanisms that promote synaptotoxicity in AD and FTLD-tau. Dr. Tracy will discuss plans to apply induced pluripotent stem cell (iPSC) technology, CRISPR-based genome editing, and proteomic mapping to answer fundamental questions about the impact of tau on synapse function in human neuronal models of tauopathy. These studies will provide unprecedented functional and mechanistic insight into the pathogenic events in human neurons that underlie memory loss in tauopathy.

Additional Details

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Map and Parking

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Event Type

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