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Trends Neurosci. 2001 Apr;24(4):219-24.

Targeting small Abeta oligomers: the solution to an Alzheimer's disease conundrum?

Author information

  • 1Northwestern University Institute for Neuroscience and Dept of Neurobiology and Physiology, Northwestern University, 2153 N Campus Drive, Evanston, IL 60208, USA. wklein@northwestern.edu

Abstract

Amyloid beta (Abeta) is a small self-aggregating peptide produced at low levels by normal brain metabolism. In Alzheimer's disease (AD), self-aggregation of Abeta becomes rampant, manifested most strikingly as the amyloid fibrils of senile plaques. Because fibrils can kill neurons in culture, it has been argued that fibrils initiate the neurodegenerative cascades of AD. An emerging and different view, however, is that fibrils are not the only toxic form of Abeta, and perhaps not the neurotoxin that is most relevant to AD: small oligomers and protofibrils also have potent neurological activity. Immuno-neutralization of soluble Abeta-derived toxins might be the key to optimizing AD vaccines that are now on the horizon.

PMID:
11250006
[PubMed - indexed for MEDLINE]
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