Amyloid β-protein oligomers and Alzheimer’s disease

Hayden, Eric Y; Teplow, David B

doi:10.1186/alzrt226

Cited by 276Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Amyloid β-protein oligomers and Alzheimer’s disease

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Hayden, Eric Y, Teplow, David B·2013·Alzheimer's Research & Therapy

DOI 10.1186/alzrt226PMC PMC3978746

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Abstract

The oligomer cascade hypothesis, which states that oligomers are the initiating pathologic agents in Alzheimer's disease, has all but supplanted the amyloid cascade hypothesis, which suggested that fibers were the key etiologic agents in Alzheimer's disease. We review here the results of in vivo, in vitro and in silico studies of amyloid β-protein oligomers, and discuss important caveats that should be considered in the evaluation of these results. This article is divided into four sections that mirror the main approaches used in the field to better understand oligomers: (1) attempts to locate and examine oligomers in vivo in situ; that is, without removing these species from their environment; (2) studies involving oligomers extracted from human or animal tissues and the subsequent characterization of their properties ex vivo; (3) studies of oligomers that have been produced synthetically and studied using a reductionist approach in relatively simple in vitro biophysical systems; and (4) computational studies of oligomers in silico. These multiple orthogonal approaches have revealed much about the molecular and cell biology of amyloid β-protein. However, as informative as these approaches have been, the amyloid β-protein oligomer system remains enigmatic.

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Misfolded Aβ and tau proteins accumulate in the AD brain in a neurodegenerative cascade leading to cognitive decline and dementia.
“Misfolded Aβ and tau proteins accumulate in the AD brain in a neurodegenerative cascade leading to cognitive decline and dementia [4,5,6,7,8,9].”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [7]
The Introduction describes Aβ deposits and oligomers in AD and links loss of cognitive function to synaptic damage and neuronal loss. The ‘Oligomer characterization in vivo’ section reports tau accumulation and cognitive decline together in a mouse model, but the paper does not establish that misfolded Aβ and tau both accumulate in the human AD brain as a single causal cascade leading to dementia. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Elevated levels of Aβ oligomers are associated with AD, as they are found in AD brains and are considered the most toxic and pathogenic form of Aβ.
“Elevated levels of oligomers have been associated with AD, as they are found in AD brains and are considered the most toxic and pathogenic form of Aβ [4,5,6,7,18].”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [7]
The Aβ oligomer hypothesis, supported by in vitro, in vivo, and ex vivo models, points to toxic Aβ oligomers rather than amyloid plaques as key players in AD pathogenesis.
“The Aβ oligomer hypothesis, supported by in vitro, in vivo, and ex vivo models, points to the toxic Aβ oligomers rather than amyloid plaques as key players in AD pathogenesis [4,5,6,7].”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [7]
Aβ oligomers are considered the most toxic and pathogenic form of Aβ.
“(AβO)s are considered the most toxic and pathogenic form of Aβ [79,82].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [82]

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3 retracted

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Authors: Hayden, E. Y., & Teplow, D. B.
Affiliations: University of California, Los Angeles (US)
Corresponding author: Teplow, David B
ORCID: Hayden, Eric Y
Teplow, David B
Venue: Alzheimer's Research & Therapy
Publisher: Springer Science and Business Media LLC
Published: 2013
Volume: 5
Issue: 6
Pages: 60
ISSN: 1758-9193 (ISSN-L)
DOI: 10.1186/alzrt226
PMC: PMC3978746
OpenAlex: W2101027386
Cited by: 276
References: 123
Citations by year: 2026: 12 · 2025: 29 · 2024: 25 · 2023: 20 · 2022: 35 · 2021: 30 · 2020: 25 · 2019: 18 · 2018: 19 · 2017: 21 · 2016: 17 · 2015: 19 · 2014: 6
FWCI: 1.54
Type: journal article
Language: en
Open access: gold
doi.org
Locations: Alzheimer s Research & Therapy (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
eScholarship (California Digital Library) (submittedVersion)
Funders: National Institutes of Health (UL1TR000124, NS038328, AG028748, AG027818)
National Institute on Aging (R01AG041295, P30AG028748)
Clinical and Translational Science Institute, University of California, Los Angeles (UL1TR000124)
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: Alzheimer's disease, amyloid hypothesis, amyloid fibrils

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Amyloid β-protein oligomers and Alzheimer’s disease

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