The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
The intersection of amyloid beta and tau in glutamatergic synaptic dysfunction and collapse in Alzheimer's disease
Open accessAbstract
The synaptic connections that form between neurons during development remain plastic and able to adapt throughout the lifespan, enabling learning and memory. However, during aging and in particular in neurodegenerative diseases, synapses become dysfunctional and degenerate, contributing to dementia. In the case of Alzheimer’s disease (AD), synapse loss is the strongest pathological correlate of cognitive decline, indicating that synaptic degeneration plays a central role in dementia. Over the past decade, strong evidence has emerged that oligomeric forms of amyloid beta, the protein that accumulates in senile plaques in the AD brain, contribute to degeneration of synaptic structure and function. More recent data indicate that pathological forms of tau protein, which accumulate in neurofibrillary tangles in the AD brain, also cause synaptic dysfunction and loss. In this review, we will present the case that soluble forms of both amyloid beta and tau protein act at the synapse to cause neural network dysfunction, and further that these two pathological proteins may act in concert to cause synaptic pathology. These data may have wide-ranging implications for the targeting of soluble pathological proteins in neurodegenerative diseases to prevent or reverse cognitive decline.
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Cites
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Cited by
The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer’s Disease
Spires-Jones, T. L., & Hyman, B. T. (2014) · Neuron · doi:10.1016/j.neuron.2014.05.004 · Cited by 1,201
Self-citationThe importance of tau phosphorylation for neurodegenerative diseases
Noble, W., Hanger, D. P., Miller, C. C. J., & Lovestone, S. (2013) · Frontiers in Neurology · doi:10.3389/fneur.2013.00083 · Cited by 475
Webers, A., Heneka, M. T., & Gleeson, P. A. (2020) · Immunology & Cell Biology · doi:10.1111/imcb.12301 · Cited by 367
The role of pathological tau in synaptic dysfunction in Alzheimer’s diseases
Wu, M., Zhang, M., Yin, X., Chen, K., Hu, Z., Zhou, Q., Cao, X., Chen, Z., & Liu, D. (2021) · Translational Neurodegeneration · doi:10.1186/s40035-021-00270-1 · Cited by 241
Meftah, S., & Gan, J. (2023) · Frontiers in Synaptic Neuroscience · doi:10.3389/fnsyn.2023.1129036 · Cited by 205
Metadata
- Authors
- Crimins, J. L., Pooler, A., Polydoro, M., Luebke, J. I., & Spires-Jones, T. L.
- Venue
- Ageing Research Reviews
- Publisher
- Elsevier BV
- Published
- 2013-06
- Volume
- 12
- Issue
- 3
- Pages
- 757-763
- ISSN
- 1568-1637 (ISSN-L)
- OpenAlex
- W2147292139
- Cited by
- 163
- References
- 41
- FWCI
- 2.34
- Type
- journal article
- Language
- en
- Open access
- green
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- Crimins, J. L., Pooler, A., Polydoro, M., Luebke, J. I., & Spires-Jones, T. L. (2013). The intersection of amyloid beta and tau in glutamatergic synaptic dysfunction and collapse in Alzheimer's disease. Ageing Research Reviews. https://doi.org/10.1016/j.arr.2013.03.002
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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