Intracellular accumulation of amyloid-beta – a predictor for synaptic dysfunction and neuron loss in Alzheimer’s disease
Open accessAbstract
Despite of long-standing evidence that beta-amyloid (Abeta) peptides have detrimental effects on synaptic function, the relationship between Abeta, synaptic and neuron loss is largely unclear. During the last years there is growing evidence that early intraneuronal accumulation of Abeta peptides is one of the key events leading to synaptic and neuronal dysfunction. Many studies have been carried out using transgenic mouse models of Alzheimer's disease (AD) which have been proven to be valuable model systems in modern AD research. The present review discusses the impact of intraneuronal Abeta accumulation on synaptic impairment and neuron loss and provides an overview of currently available AD mouse models showing these pathological alterations.
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Intraneuronal Aβ accumulation may be an important proximal neurotoxic event in AD pathogenesis.
“recent evidence indicates that intraneuronal A accumulation may be an important proximal neurotoxic event in AD pathogenesis (for review see Ref. 56,57).”
From APOE4-specific Changes in Aβ Accumulation in a New Transgenic Mouse Model of Alzheimer Disease (2012) · cites this paper as [57]
Long postmortem intervals could be a confounding factor in the evaluation of intracellular Aβ in human material.
“Long postmortem intervals could also be another confounding factor in the evaluation of this feature in human material, as compared to its detection in mice, in which samples are collected and rapidly fixed by transcardial perfusion in a well-controlled manner [6].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [6]
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References 110 · Cited by 252
- Authors
- Bayer
- Affiliations
- University of Göttingen (DE)
- Corresponding author
- Bayer
- Venue
- Frontiers in Aging Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2010
- Volume
- 2
- Pages
- 8-8
- ISSN
- 1663-4365 (ISSN-L)
- PMC
- PMC2879032
- OpenAlex
- W2045978578
- Cited by
- 252
- References
- 110
- Citations by year
- 2026: 6 · 2025: 15 · 2024: 19 · 2023: 22 · 2022: 22 · 2021: 19 · 2020: 17 · 2019: 11 · 2018: 19 · 2017: 8 · 2016: 18 · 2015: 11 · 2014: 9 · 2013: 13 · 2012: 19
- FWCI
- 11.92
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Aging Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- GoeScholar The Publication Server of the Georg-August-Universität Göttingen (Georg-August-Universität Göttingen) (submittedVersion, cc-by-nc)
- Funders
- Alzheimer Forschung Initiative
- European Commission (MEST-CT-2005-020013)
- Fritz Thyssen Stiftung
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- amyloid-beta, synaptic dysfunction, neuronal loss, Alzheimer's disease, transgenic mouse model, neurodegeneration
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