Targeting small A β oligomers: The solution to an Alzheimer's disease conundrum?

William L. Klein*, Grant A. Krafft, Caleb E. Finch

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

881 Scopus citations

Abstract

Amyloid β (Aβ) is a small self-aggregating peptide produced at low levels by normal brain metabolism. In Alzheimer's disease (AD), self-aggregation of A β 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 A β, and perhaps not the neurotoxin that is most relevant to AD: small oligomers and protofibrils also have potent neurological activity. Immuno-neutralization of soluble A β-derived toxins might be the key to optimizing AD vaccines that are now on the horizon.

Original languageEnglish (US)
Pages (from-to)219-224
Number of pages6
JournalTrends in Neurosciences
Volume24
Issue number4
DOIs
StatePublished - Apr 1 2001

ASJC Scopus subject areas

  • Neuroscience(all)

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