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Tau-targeting therapies for Alzheimer disease: current status and future directions
Open accessAbstract
Alzheimer disease (AD) is the most common cause of dementia in older individuals. AD is characterized pathologically by amyloid-β (Aβ) plaques and tau neurofibrillary tangles in the brain, with associated loss of synapses and neurons, which eventually results in dementia. Many of the early attempts to develop treatments for AD focused on Aβ, but a lack of efficacy of these treatments in terms of slowing disease progression led to a change of strategy towards targeting of tau pathology. Given that tau shows a stronger correlation with symptom severity than does Aβ, targeting of tau is more likely to be efficacious once cognitive decline begins. Anti-tau therapies initially focused on post-translational modifications, inhibition of tau aggregation and stabilization of microtubules. However, trials of many potential drugs were discontinued because of toxicity and/or lack of efficacy. Currently, the majority of tau-targeting agents in clinical trials are immunotherapies. In this Review, we provide an update on the results from the initial immunotherapy trials and an overview of new therapeutic candidates that are in clinical development, as well as considering future directions for tau-targeting therapies.
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“Research has indicated that tau pathology has a stronger correlation with cognitive deficits than Aβ plaques, indicating that treatment benefits from targeting tau may outweigh those from concentrating only on amyloid clearance [94,95].”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [94]
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Metadata
- Authors
- Congdon, E. E., Ji, C., Tetlow, A. M., Jiang, Y., & Sigurdsson, E. M.
- Affiliations
- New York University (US)
- NYU Langone Health (US)
- Corresponding author
- Sigurdsson, Einar M.
- Venue
- Nature Reviews Neurology
- Published
- 2023-10-24
- Volume
- 19
- Issue
- 12
- Pages
- 715-736
- ISSN
- 1759-4758 (ISSN-L)
- 1759-4766
- PMC
- PMC10965012
- OpenAlex
- W4387904363
- Cited by
- 371
- References
- 380
- Citations by year
- 2026: 125 · 2025: 170 · 2024: 74 · 2023: 1
- FWCI
- 13.17
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Reviews Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Alzheimer's Association (AG032611, AARF-22-924783)
- National Institutes of Health (NS120488)
- National Institute on Aging (R21AG069475, R01AG032611, T32AG052909)
- National Institute of Neurological Disorders and Stroke (RF1NS120488, R01NS120488, R01NS077239)
- 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, tau protein, tau immunotherapy, tau aggregation, microtubule stabilization, post-translational modification, amyloid plaques, neurofibrillary tangles, clinical trials, drug candidates
- MeSH terms
- Aged, Alzheimer Disease, Humans, Immunotherapy, Amyloid beta-Peptides, Neurofibrillary Tangles, tau Proteins, Plaque, Amyloid
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