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Trends Cogn Sci. 2011 Nov;15(11):520-6. doi: 10.1016/j.tics.2011.09.004. Epub 2011 Oct 7.

Lifespan brain activity, β-amyloid, and Alzheimer's disease.

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  • 1Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, CA 94720, USA. jagust@berkeley.edu

Abstract

Alzheimer's disease (AD) is the most common cause of progressive cognitive decline and dementia in adults. While the amyloid cascade hypothesis of AD posits an initiating role for the β-amyloid (Aβ) protein, there is limited understanding of why Aβ is deposited. A growing body of evidence based on in vitro, animal studies and human imaging work suggests that synaptic activity increases Aβ, which is deposited preferentially in multimodal brain regions that show continuous levels of heightened activation and plasticity across the lifespan. Imaging studies of people with genetic predispositions to AD are consistent with these findings, suggesting a mechanism whereby neural efficiency or cognitive reserve may diminish Aβ deposition. The aggregated findings unify observations from cellular and molecular studies with human cognitive neuroscience to reveal potential mechanisms of AD development.

PMID:
21983147
PMCID:
PMC3206968
DOI:
10.1016/j.tics.2011.09.004
[PubMed - indexed for MEDLINE]
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