Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 175, Issue 5, Pages 1810-1816Publisher
ELSEVIER SCIENCE INC
DOI: 10.2353/ajpath.2009.090219
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Funding
- National Institutes of Health [HD83062, NS11766, GM45735, GM66037, CA13696, GM61721, AG05136, AG08702]
- John Douglas French Alzheimer Foundation
- Veterans Administration Research Funds
- American Health Assistance Foundation
- Muscular Dystrophy Association
- Marriott Foundation
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Presenilin-1 (PSI) and -2 (PS2), which when mutated cause familial Alzheimer disease, have been localized to numerous compartments of the cell, including the endoplasmic reticulum, Golgi, nuclear envelope, endosomes, lysosomes, the plasma membrane, and mitochondria. Using three complementary approaches, subcellular fractionation, gamma-secretase activity assays, and immunocytochemistry, we show that presenilins are highly enriched in a subcompartment of the endoplasmic reticulum that is associated with mitochondria and that forms a physical bridge between the two organelles, called endoplasmic reticulum-mitochondria-associated membranes. A localization of PSI and PS2 in mitochondria-associated membranes may help reconcile the disparate hypotheses regarding the pathogenesis of Alzheimer disease and may explain many seemingly unrelated features of this devastating neurodegenerative disorder. (Am J Pathol 2009, 175:1810-1816; DOI: 10.2353/ajpath.2009.090219)
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