Stanford Neurosciences Institute Seminar Series Presents
Presenilins and Alzheimer’s disease: new insight into the pathogenic mechanism
Jie Shen, Ph.D.
Professor of Neurology, Harvard Medical School Center for Neurological Diseases
Host: Aaron Gitler
Presenilin constitutes the catalytic subunit of gamma-secretase and is the major genetic hotspot for familial Alzheimer’s disease, harboring ~90% of causative mutations. We employed gene targeting and multidisciplinary analysis in a series of mouse models to elucidate the normal functions of Presenilin and how these functions are perturbed by pathogenic mutations. I will present our unexpected findings and discuss their implications for understanding disease mechanisms and devising effective therapeutic strategies.
 Presenilin-1 Knockin Mice Reveal Loss-of-Function Mechanism for Familial Alzheimer's Disease. Dan Xia, Hirotaka Watanabe, Jie Shen, Raymond Kelleher lll Neuron. 2015 Mar 4;85(5):967-81. doi:10.1016/j.neuron.2015.02.010
 Presenilins are essential for regulating neurotrasnmitter release. Chen Zhang, Bei Wu, Vassilios Beglopoulos, Mary Wines-Samuelson, Dawei Zhang, Ioannis Dragatsis, Thomas C. Südhof, Jei Shen Nature. 2009 May 27;460:632-36. doi:10.1038/nature08177