Synaptic dysfunction in Alzheimer's disease: Mechanisms and therapeutic strategies
Abstract
Alzheimer's disease (AD), the most prevalent neurodegenerative disease in the elderly population, is characterized by progressive cognitive decline and pathological hallmarks of amyloid plaques and neurofibrillary tangles. However, its pathophysiological mechanisms are poorly understood, and diagnostic tools and interventions are limited. Here, we review recent research on the amyloid hypothesis and beta-amyloid-induced dysfunction of neuronal synapses through distinct cell surface receptors. We also review how tau protein leads to synaptotoxicity through pathological modification, localization, and propagation. Finally, we discuss experimental therapeutics for AD and propose potential applications of disease-modifying strategies targeting synaptic failure for improved treatment of AD.
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Newly developed molecules target amyloid and tau proteins.
“These newly developed molecules target the amyloid and tau proteins [97].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [97]
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References 194 · Cited by 258
- Authors
- Chen, Y., Fu, A. K. Y., & Ip, N. Y.
- Affiliations
- Chinese Academy of Sciences (CN)
- Hong Kong University of Science and Technology (HK)
- Corresponding author
- Chen, Yu
- Ip, Nancy Y.
- Venue
- Pharmacology & Therapeutics
- Publisher
- Elsevier BV
- Published
- 2019-03
- Volume
- 195
- Pages
- 186-198
- ISSN
- 0163-7258 (ISSN-L)
- OpenAlex
- W2901147556
- Cited by
- 258
- References
- 194
- Citations by year
- 2026: 38 · 2025: 45 · 2024: 35 · 2023: 29 · 2022: 35 · 2021: 44 · 2020: 18 · 2019: 13 · 2017: 1
- FWCI
- 2.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Pharmacology & Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Funders
- Hong Kong Research Council Theme-based Research Schemes (T13/605–18-W)
- Shenzhen Knowledge Innovation Program (JCYJ20151030140325152, JCYJ20160428145818099, JCYJ20170413165053031, JCYJ20151030154629774)
- Areas of Excellence Scheme of the University Grants Committee (AoE/M-604/16)
- Research Grants Council of Hong Kong SAR (C6003-14G)
- National Natural Science Foundation of China (31671047)
- External Cooperation Program of Chinese Academy of Sciences (172644KYSB20160026)
- S.H. Ho Foundation
- University Lodge of Hong Kong (ULHK15SC01)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, synaptic dysfunction, amyloid hypothesis, amyloid-beta, synaptotoxicity, tau protein, cell surface receptors, amyloid plaques, neurofibrillary tangles, disease-modifying therapy, cognitive decline
- MeSH terms
- Alzheimer Disease, Animals, Cognition, Humans, Synapses, Amyloid beta-Peptides, tau Proteins
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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