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Interaction between Aβ and Tau in the Pathogenesis of Alzheimer’s Disease
Open accessAbstract
Extracellular neuritic plaques composed of amyloid‑β (Aβ) protein and intracellular neurofibrillary tangles containing phosphorylated tau protein are the two hallmark proteins of Alzheimer's disease (AD), and the separate neurotoxicity of these proteins in AD has been extensively studied. However, interventions that target Aβ or tau individually have not yielded substantial breakthroughs. The interest in the interactions between Aβ and tau in AD is increasing, but related drug investigations are in their infancy. This review discusses how Aβ accelerates tau phosphorylation and the possible mechanisms and pathways by which tau mediates Aβ toxicity. This review also describes the possible synergistic effects between Aβ and tau on microglial cells and astrocytes. Studies suggest that the coexistence of Aβ plaques and phosphorylated tau is related to the mechanism by which Aβ facilitates the propagation of tau aggregation in neuritic plaques. The interactions between Aβ and tau mediate cognitive dysfunction in patients with AD. In summary, this review summarizes recent data on the interplay between Aβ and tau to promote a better understanding of the roles of these proteins in the pathological process of AD and provide new insights into interventions against AD.
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“For instance, Aβ oligomers promote tau phosphorylation and mislocalization by activating kinases such as GSK-3, CDK5, and Fyn kinase, and by interfering with tau degradation [50].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [50]
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“Through the cellular prion protein/mGluR5 complex, Aβ oligomers can trigger Fyn kinase activation, further driving tau toxicity [50].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [50]
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“Since amyloid-beta (Aβ) plaques and tau tangles are characteristic of AD and are thought to be important in the onset and development of the disease, the main focus of these therapies has been on removing or reducing them.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [84]
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Metadata
- Authors
- Zhang, H., Wei, W., Zhao, M., Ma, L., Jiang, X., Pei, H., Cao, Y., & Li, H.
- Affiliations
- Xiyuan Hospital (CN)
- Beijing University of Chinese Medicine (CN)
- Corresponding author
- Cao, Yu
- Li, Hao
- Venue
- International Journal of Biological Sciences
- Publisher
- Ivyspring International Publisher
- Published
- 2021
- Volume
- 17
- Issue
- 9
- Pages
- 2181-2192
- ISSN
- 1449-2288 (ISSN-L)
- PMC
- PMC8241728
- OpenAlex
- W3166313369
- Cited by
- 689
- References
- 185
- Citations by year
- 2026: 182 · 2025: 268 · 2024: 141 · 2023: 73 · 2022: 22 · 2021: 3
- FWCI
- 37.38
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- International Journal of Biological Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81873350, 7202174)
- National Science and Technology Major Project
- 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, tau protein, tau phosphorylation, neuritic plaques, neurofibrillary tangles, microglia, astrocytes, tau aggregation, cognitive impairment, neurotoxicity
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Humans, Phosphorylation, Amyloid beta-Peptides, tau Proteins
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