学术报告: Presenilin Function in Health and Alzheimer's Disease
Speaker: Prof. Sangram S. Sisodia
Department of Neurobiology
University of Chicago
Host: Prof. Yigong Shi
Date: 10:00AM-11:00AM, Apr. 20th (Friday)
Venue: 143, New Biology Building，Tsinghua University
Abstract:
Inheritance of mutant PSEN genes encoding presenilins (PS1 and PS2) variants cause autosomal dominant, familial Alzheimer's disease (FAD). PS is the catalytic subunit of the γ-secretase complex that is essential for intramembranous processing of APP, Notch and several type I membrane proteins and I will present studies aimed at elucidating the structure and activity of the γ-secretase complex. In addition, I will summarize a series of experiments that test the proposal that presenilins play a role in autophagy. Finally, studies will be presented that extend our earlier findings that expression of FAD-linked PS1 variants exhibit impairments in enrichment-mediated proliferation and neurogenic differentiation of hippocampal progenitors in a non-cell autonomous manner. In this regard, I will describe the analysis of a transgenic line in which an FAD-linked PSEN transgene can be conditionally inactivated in a cell-specific and/or temporal manner to assess enrichment-mediated effects of FAD-linked PS1 variants on NPC phenotypes in in vivo settings.
Supported by NIH AG027854 (SSS), Alzheimer’s Association, AHAF, the Edward H. Levi Fund, Adler Foundation and Cure Alzheimer’s Fund (CAF). SSS is a paid Consultant of Nociris, Inc.and Eisai Research Labs Inc.
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