Participation of Presenilin 2 in apoptosis: Enhanced basal activity conferred by an Alzheimer mutation

Benjamin Wolozin, Katsunori Iwasaki, Pasquale Vito, J. Kelly Ganjei, Emanuela Lacanà, Trey Sunderland, Boyu Zhao, John W. Kusiak, Wilma Wasco, Luciano D'Adamio

Research output: Contribution to journalArticlepeer-review

392 Scopus citations


Overexpression of the familial Alzheimer's disease gene Presenilin 2 (PS2) in nerve growth factor-differentiated PC12 cells increased apoptosis induced by trophic factor withdrawal or β-amyloid. Transfection of antisense PS2 conferred protection against apoptosis induced by trophic withdrawal in nerve growth factor-differentiated or amyloid precursor protein-expressing PC12 cells. The apoptotic cell death induced by PS2 protein was sensitive to pertussis toxin, suggesting that heterotrimeric GTP-binding proteins are involved. A PS2 mutation associated with familial Alzheimer's disease was found to generate a molecule with enhanced basal apoptotic activity. This gain of function might accelerate the process of neurodegeneration that occurs in Alzheimer's disease, leading to the earlier age of onset characteristic of familial Alzheimer's disease.

Original languageEnglish (US)
Pages (from-to)1710-1712
Number of pages3
Issue number5293
StatePublished - Dec 6 1996
Externally publishedYes

ASJC Scopus subject areas

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