Tau-targeting therapy in Alzheimer’s disease: Critical advances and future opportunities
Open accessAbstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by two pathological hallmark lesions: extracellular plaques composed of β-amyloid (Aβ) peptide and intracellular neurofibrillary tangles made up of highly phosphorylated tau protein. Over the past two decades, most disease-modifying therapies against AD have been developed mainly on the basis of the amyloid cascade hypothesis with a focus on Aβ. However, these agents yielded only limited benefits against disease progression, which prompts us to revitalize the long-neglected tau hypothesis. Tau protein is a microtubule-associated protein, which can stabilize microtubules, regulate microtubule assembly, and affect the morphology and growth of neuronal axons. Much more importantly, the degree of tau pathology is more closely related to cognitive decline in AD patients than that of Aβ pathology. Therefore, tau-targeting therapy seems to be a promising approach to combat AD. This review describes the research progress of tau-targeting therapy in AD, with an emphasis on immunotherapy. The current challenges and future perspectives in this field are also discussed.
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In clinical trials, immunotherapies make up the majority of tau-targeting treatments.
“In clinical trials, immunotherapies make up the majority of tau-targeting treatments.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [96]
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Research works printed but not linked: 1
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Tau-targeting therapies for Alzheimer disease: Current status and future directions
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Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease
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- Authors
- Guo, Y., Li, S., Zeng, L.-H., & Tan, J.
- Affiliations
- Guiyang Medical University (CN)
- First Affiliated Hospital of Dalian Medical University (CN)
- Corresponding author
- Tan, Jun
- Venue
- Ageing and Neurodegenerative Diseases
- Publisher
- OAE Publishing Inc.
- Published
- 2022
- Volume
- 2
- Issue
- 3
- Pages
- 11
- ISSN
- 2769-5301 (ISSN-L)
- OpenAlex
- W4286480258
- Cited by
- 61
- References
- 222
- Citations by year
- 2026: 6 · 2025: 20 · 2024: 16 · 2023: 16 · 2022: 3
- FWCI
- 8.51
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Ageing and Neurodegenerative Diseases (publishedVersion, cc-by)
- Funders
- High-level Talent Foundation of Guizhou Medical University (YJ19017, HY2020, J.T.)
- National Natural Science Foundation of China (NSFC) (82171423, 82060211, J.T.)
- Topics
- Health Sciences › Medicine › Physiology › 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, tau protein, tau hypothesis, tau immunotherapy, amyloid hypothesis, neurofibrillary tangles, tau phosphorylation, microtubule stabilization, cognitive decline
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
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