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Soluble amyloid-β oligomers as synaptotoxins leading to cognitive impairment in Alzheimer’s disease
Open accessAbstract
Alzheimer's disease (AD) is the most common form of dementia in the elderly, and affects millions of people worldwide. As the number of AD cases continues to increase in both developed and developing countries, finding therapies that effectively halt or reverse disease progression constitutes a major research and public health challenge. Since the identification of the amyloid-β peptide (Aβ) as the major component of the amyloid plaques that are characteristically found in AD brains, a major effort has aimed to determine whether and how Aβ leads to memory loss and cognitive impairment. A large body of evidence accumulated in the past 15 years supports a pivotal role of soluble Aβ oligomers (AβOs) in synapse failure and neuronal dysfunction in AD. Nonetheless, a number of basic questions, including the exact molecular composition of the synaptotoxic oligomers, the identity of the receptor(s) to which they bind, and the signaling pathways that ultimately lead to synapse failure, remain to be definitively answered. Here, we discuss recent advances that have illuminated our understanding of the chemical nature of the toxic species and the deleterious impact they have on synapses, and have culminated in the proposal of an Aβ oligomer hypothesis for Alzheimer's pathogenesis. We also highlight outstanding questions and challenges in AD research that should be addressed to allow translation of research findings into effective AD therapies.
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“It is worth noting that SCFAs interfere with protein-protein interactions between amyloid-β peptides (Aβ), thereby disrupting their assembly into neurotoxic oligomers (34), the main toxins responsible for synapse dysfunction and cognitive deficits in AD (164).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [164]
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The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication
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Metadata
- Authors
- Ferreira, S. T., Lourenco, M. V., Oliveira, M. M., & De Felice, F. G.
- Affiliations
- Universidade Federal do Rio de Janeiro (BR)
- Corresponding author
- Ferreira, Sergio T.
- Venue
- Frontiers in Cellular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2015-05-26
- Volume
- 9
- Pages
- 191-191
- ISSN
- 1662-5102 (ISSN-L)
- PMC
- PMC4443025
- OpenAlex
- W1520284233
- Cited by
- 373
- References
- 254
- Citations by year
- 2026: 23 · 2025: 24 · 2024: 16 · 2023: 40 · 2022: 38 · 2021: 51 · 2020: 45 · 2019: 33 · 2018: 40 · 2017: 38 · 2016: 23 · 2015: 2
- FWCI
- 4.22
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- Conselho Nacional de Desenvolvimento Científico e Tecnológico
- Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro
- Institute for Translational Neuroscience
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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-beta oligomers, synaptotoxicity, cognitive impairment, amyloid plaques, neuronal dysfunction, memory loss, Alzheimer's disease pathogenesis, Alzheimer's disease treatment
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