The DOI matches its Crossref record; 349 of the 349 references it cites were found in a registry or an index.
Amyloid-Beta and Phosphorylated Tau Accumulations Cause Abnormalities at Synapses of Alzheimer’s disease Neurons
Open accessAbstract
Amyloid-beta (Aβ) and hyperphosphorylated tau are hallmark lesions of Alzheimer’s disease (AD). However, the loss of synapses and dysfunctions of neurotransmission are more directly tied to disease severity. The role of these lesions in the pathoetiological progression of the disease remains contested. Biochemical, cellular, molecular, and pathological studies provided several lines of evidence and improved our understanding of how Aβ and hyperphosphorylated tau accumulation may directly harm synapses and alter neurotransmission. In vitro evidence suggests that Aβ and hyperphosphorylated tau have both direct and indirect cytotoxic effects that affect neurotransmission, axonal transport, signaling cascades, organelle function, and immune response in ways that lead to synaptic loss and dysfunctions in neurotransmitter release. Observations in preclinical models and autopsy studies support these findings, suggesting that while the pathoetiology of positive lesions remains elusive, their removal may reduce disease severity and progression. The purpose of this article is to highlight the need for further investigation of the role of tau in disease progression and its interactions with Aβ and neurotransmitters alike.
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2 retracted
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Self-citationJeremic, D., Jiménez-Díaz, L., & Navarro-López, J. D. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101496 · Cited by 306
Astrocyte Senescence and Alzheimer’s Disease: A Review
Han, X., Zhang, T., Liu, H., Mi, Y., & Gou, X. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00148 · Cited by 177
Alzheimer’s Disease: Exploring the Landscape of Cognitive Decline
Tenchov, R., Sasso, J. M., & Zhou, Q. A. (2024) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.4c00339 · Cited by 170
Role of natural products for the treatment of Alzheimer’s disease
Noori, T., Dehpour, A. R., Sureda, A., Sobarzo-Sanchez, E., & Shirooie, S. (2021) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2021.173974 · Cited by 141
Metadata
- Authors
- Rajmohan, R., & Reddy, P. H.
- Venue
- Journal of Alzheimer’s Disease
- Publisher
- SAGE Publications
- Published
- 2016-08-26
- Volume
- 57
- Issue
- 4
- Pages
- 975-999
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W2510053021
- Cited by
- 688
- References
- 349
- FWCI
- 7.76
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Amyloid-Beta and Phosphorylated Tau Accumulations Cause Abnormalities at Synapses of Alzheimer’s disease Neurons. https://app.cochat.ai/papers/10.3233/jad-160612
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- Rajmohan, R., & Reddy, P. H. (2017). Amyloid-Beta and Phosphorylated Tau Accumulations Cause Abnormalities at Synapses of Alzheimer’s disease Neurons. Journal of Alzheimer’s Disease. https://doi.org/10.3233/jad-160612
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
