Tau Post-translational Modifications: Dynamic Transformers of Tau Function, Degradation, and Aggregation
Open accessAbstract
Post-translational modifications (PTMs) on tau have long been recognized as affecting protein function and contributing to neurodegeneration. The explosion of information on potential and observed PTMs on tau provides an opportunity to better understand these modifications in the context of tau homeostasis, which becomes perturbed with aging and disease. Prevailing views regard tau as a protein that undergoes abnormal phosphorylation prior to its accumulation into the toxic aggregates implicated in Alzheimer's disease (AD) and other tauopathies. However, the phosphorylation of tau may, in fact, represent part of the normal but interrupted function and catabolism of the protein. In addition to phosphorylation, tau undergoes another forms of post-translational modification including (but not limited to), acetylation, ubiquitination, glycation, glycosylation, SUMOylation, methylation, oxidation, and nitration. A holistic appreciation of how these PTMs regulate tau during health and are potentially hijacked in disease remains elusive. Recent studies have reinforced the idea that PTMs play a critical role in tau localization, protein-protein interactions, maintenance of levels, and modifying aggregate structure. These studies also provide tantalizing clues into the possibility that neurons actively choose how tau is post-translationally modified, in potentially competitive and combinatorial ways, to achieve broad, cellular programs commensurate with the distinctive environmental conditions found during development, aging, stress, and disease. Here, we review tau PTMs and describe what is currently known about their functional impacts. In addition, we classify these PTMs from the perspectives of protein localization, electrostatics, and stability, which all contribute to normal tau function and homeostasis. Finally, we assess the potential impact of tau PTMs on tau solubility and aggregation. Tau occupies an undoubtedly important position in the biology of neurodegenerative diseases. This review aims to provide an integrated perspective of how post-translational modifications actively, purposefully, and dynamically remodel tau function, clearance, and aggregation. In doing so, we hope to enable a more comprehensive understanding of tau PTMs that will positively impact future studies.
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The goal of tau treatments is to prevent tau from aggregating and spreading.
“The goal of tau treatments is to prevent tau from aggregating and spreading.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [199]
Numerous approaches, such as tau aggregation inhibitors, are being studied to address the tau protein problem and prevent tau tangle formation.
“Numerous approaches, such as tau aggregation inhibitors, are being studied in an effort to address the tau protein problem and prevent tau tangle formation.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [199]
The accumulation of tau protein in neurofibrillary tangles, known as tau protein modulation, provides a novel venue for disease modification.
“The accumulation of tau protein in neurofibrillary tangles, which is known as tau protein modulation, provides a novel venue for disease modification.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [199]
Techniques for tau immunotherapy, such as those being tried with AADvac1, function by teaching the immune system to eliminate aberrant tau proteins from the brain.
“Techniques for tau immunotherapy, such as those being tried with AADvac1, function by teaching the immune system to eliminate aberrant tau proteins from the brain.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [199]
There is evidence that tau vaccinations may slow the disease's course by reducing tau protein accumulation.
“First, there is evidence that tau vaccinations may slow the disease’s course by reducing tau protein accumulation [198,199,200,201].”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [199]
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References 316 · Cited by 367
- Authors
- Alquezar, C., Arya, S., & Kao, A. W.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- Kao, Aimee W.
- Venue
- Frontiers in Neurology
- Publisher
- Frontiers Media SA
- Published
- 2021-01-07
- Volume
- 11
- Pages
- 595532-595532
- ISSN
- 1664-2295 (ISSN-L)
- PMC
- PMC7817643
- OpenAlex
- W3119598339
- Cited by
- 367
- References
- 316
- Citations by year
- 2026: 60 · 2025: 85 · 2024: 72 · 2023: 57 · 2022: 62 · 2021: 30
- FWCI
- 7.38
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Neurology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health
- 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
- tau protein, post-translational modification, tau phosphorylation, tau acetylation, ubiquitination, glycation, glycosylation, SUMOylation, methylation, oxidation, nitration, tau aggregation, tau clearance, protein-protein interaction, protein localization, neurodegeneration, Alzheimer's disease, tauopathy
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