Cited by 989Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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

Klein, W·2001·Trends in Neurosciences

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.

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Crossref · 10.1016/s0166-2236(00)01749-5

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Authors
Klein, W.
Affiliations
Northwestern University (US)
Corresponding author
Klein, W
Venue
Trends in Neurosciences
Publisher
Elsevier BV
Published
2001-04-01
Volume
24
Issue
4
Pages
219-224
ISSN
0166-2236 (ISSN-L)
OpenAlex
W1972567838
Cited by
989
References
47
Citations by year
2026: 5 · 2025: 4 · 2024: 26 · 2023: 19 · 2022: 16 · 2021: 19 · 2020: 29 · 2019: 21 · 2018: 29 · 2017: 36 · 2016: 38 · 2015: 39 · 2014: 40 · 2013: 39 · 2012: 71
FWCI
31.88
Type
journal article
Language
en
Open access
closed
Locations
  • Trends in Neurosciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1p01ag015501-01)
  • National Institute on Aging (AG-13499, AG-15501, R01AG013499)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
amyloid-beta, Alzheimer's disease, protofibrils, amyloid fibrils, neurotoxicity, amyloid plaques, neurodegeneration, immunization, Alzheimer's disease vaccine, peptide self-aggregation
MeSH terms
Alzheimer Disease, Animals, Antibodies, Hippocampus, Mice, Transgenic, Peptide Fragments, Vaccines, Signal Transduction, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Synaptophysin, Long-Term Potentiation, Mice, Plaque, Amyloid

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