Amyloid beta mediates memory formation
- 1Department of Neuroscience, Mount Sinai School of Medicine, New York, New York 10029, USA;
- 2Department of Psychiatry, Mount Sinai School of Medicine, New York, New York 10029, USA
Abstract
The amyloid precursor protein (APP) undergoes sequential cleavages to generate various polypeptides, including the amyloid β (1–42) peptide (Aβ[1–42]), which is believed to play a major role in amyloid plaque formation in Alzheimer's disease (AD). Here we provide evidence that, in contrast with its pathological role when accumulated, endogenous Aβ in normal hippocampi mediates learning and memory formation. Furthermore, hippocampal injection of picomolar concentrations of exogenous Aβ(1–42) enhances memory consolidation. Correlative data suggest that Aβ peptides may exert their function via nicotinic acethylcoline receptors. Hence, Aβ peptides, including Aβ(1–42), play an important physiological role in hippocampal memory formation.
Footnotes
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↵3 Present address: CIMA, University of Navarra, CIBERNED, Pamplona 31008, Spain.
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↵4 Corresponding author.
↵E-mail cristina.alberini{at}mssm.edu; fax (212) 996-9785.
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Article is online at http://www.learnmem.org/cgi/doi/10.1101/lm.1310209.
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- Received December 15, 2008.
- Accepted February 17, 2009.
- Copyright © 2009 by Cold Spring Harbor Laboratory Press
