Soluble Aβ oligomer production and toxicity

Larson, Megan E.; Lesné, Sylvain E.

doi:10.1111/j.1471-4159.2011.07478.x

Cited by 356Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Soluble Aβ oligomer production and toxicity

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Larson, Megan E., Lesné, Sylvain E.·2012·Journal of Neurochemistry

DOI 10.1111/j.1471-4159.2011.07478.xPMC PMC3254782

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Abstract

For nearly 100 years following the first description of this neurological disorder by Dr Alois Alzheimer, amyloid plaques and neurofibrillary tangles have been hypothesized to cause neuronal loss. With evidence that the extent of insoluble, deposited amyloid poorly correlated with cognitive impairment, research efforts focused on soluble forms of Aβ, also referred as Aβ oligomers. Following a decade of studies, soluble oligomeric forms of Aβ are now believed to induce the deleterious cascade(s) involved in the pathophysiology of Alzheimer's disease. In this review, we will discuss our current understanding about endogenous oligomeric Aβ production, their relative toxicity in vivo and in vitro, and explore the potential future directions needed for the field.

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In FAD-Tg mice, soluble oAβ reduces synaptic plasticity.
“reduces synaptic plasticity”
From APOE4-specific Changes in Aβ Accumulation in a New Transgenic Mouse Model of Alzheimer Disease (2012) · cites this paper as [52]
The Toxicity of Oligomeric Aβ Assemblies section (page unavailable) says oligomeric Aβ can impair synaptic plasticity. It also discusses Aβ oligomers and deficits in transgenic mouse models, but the passages do not establish that soluble oligomers reduced synaptic plasticity specifically in those mice; the mouse-model findings described concern cognition or neuronal function. (LLM, conf=0.82)
Experimental — accuracy not yet measured
In FAD-Tg mice, soluble oAβ suppresses synaptic function.
“In FAD-Tg mice, soluble oA␤ suppresses synaptic function”
From APOE4-specific Changes in Aβ Accumulation in a New Transgenic Mouse Model of Alzheimer Disease (2012) · cites this paper as [52]
In ‘II. Toxicity of Oligomeric Aβ Assemblies’ (page unavailable), the review reports that soluble Aβ oligomers inhibit LTP, a measure of synaptic plasticity. It also describes Aβ-induced neuronal and cognitive deficits in APP-transgenic mice, but does not clearly establish that soluble oligomers suppress synaptic function specifically in those mice. (LLM, conf=0.80)
Experimental — accuracy not yet measured
In FAD-Tg mice, soluble oAβ impairs learning and memory.
“impairs learning and memory (52).”
From APOE4-specific Changes in Aβ Accumulation in a New Transgenic Mouse Model of Alzheimer Disease (2012) · cites this paper as [52]

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RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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“Supporting this hypothesis, larger Ab oligomers detected in mice, such as potential hexamers ( 27 kDa) and Ab*56, are formed at ages following the formation of trimers and prior to plaque formation in Tg2576 (Lesne et al. 2006).”
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RETRACTED: Cognitive effects of cell-derived and synthetically derived Aβ oligomers
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Authors: Larson, M. E., & Lesné, S. E.
Affiliations: University of Minnesota (US)
Corresponding author: Lesné, Sylvain E.
ORCID: Larson, Megan E.
Lesné, Sylvain E.
Venue: Journal of Neurochemistry
Publisher: Wiley
Published: 2011-11-28
Volume: 120
Issue: s1
Pages: 125-139
ISSN: 0022-3042 (ISSN-L)
1471-4159
DOI: 10.1111/j.1471-4159.2011.07478.x
PMC: PMC3254782
OpenAlex: W1553011341
Cited by: 356
References: 90
Citations by year: 2026: 8 · 2025: 9 · 2024: 17 · 2023: 13 · 2022: 10 · 2021: 26 · 2020: 25 · 2019: 20 · 2018: 20 · 2017: 37 · 2016: 38 · 2015: 36 · 2014: 41 · 2013: 36 · 2012: 19
FWCI: 3.29
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Journal of Neurochemistry (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: University of Minnesota Foundation
National Institutes of Health
National Institute on Aging (R00AG031293)
National Institute of Neurological Disorders and Stroke (R01NS033249)
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 oligomers, soluble amyloid-beta, Alzheimer's disease, oligomer toxicity, amyloid plaques, neurofibrillary tangles, neuronal loss, cognitive impairment
MeSH terms: Alzheimer Disease, Animals, Humans, Solubility, Amyloid beta-Peptides, Neurofibrillary Tangles, Plaque, Amyloid

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Soluble Aβ oligomer production and toxicity

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