ReviewBiology2021
Tau Post-Translational Modifications: Potentiators of Selective Vulnerability in Sporadic Alzheimer's Disease.
Review in Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Tau-mediated Mechanisms in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Tunable tau expression in C. elegans neurons reveals that early-AD tau phosphorylation selectively impacts behavior and mitochondrial quality control.Neurobiology of disease · 2026Article
- Modified tau leads to neuronal and global ribosome dysfunction inbioRxiv : the preprint server for biology · 2025Article
- Patterns of phosphorylated tau accumulation in a spectrum of acquired and developmental brain lesions associated with refractory epilepsy.Epilepsia · 2025Article
- Synapse vulnerability and resilience across the clinical spectrum of dementias.Nature reviews. Neurology · 2025Review
- Uric Acid, the End-Product of Purine Metabolism, Mitigates Tau-Related Abnormalities: Comparison with DOT, a Non-Antibiotic Oxytetracycline Derivative.Biomolecules · 2025Article
- Targeting NOX inhibitors in neurodegeneration: a therapeutic perspective.Metabolic brain disease · 2025Review
- Glucose starvation induces tau phosphorylation leading to cellular stress response in fission yeast.Archives of microbiology · 2025Article
- Pathogenic oligomeric Tau alters neuronal RNA processes through the formation of nuclear heteromeric amyloids with RNA-binding protein Musashi1.Progress in neurobiology · 2025Article
- Tau-targeting nanoparticles for treatment of Alzheimer's disease.Exploration (Beijing, China) · 2025Review
- Synapse vulnerability and resilience underlying Alzheimer's disease.EBioMedicine · 2025Review
- Article
- Excessive Alcohol Use as a Risk Factor for Alzheimer's Disease: Epidemiological and Preclinical Evidence.Advances in experimental medicine and biology · 2025Review
- Selective Vulnerability to Neurodegenerative Disease: Insights from Cell Type-Specific Translatome Studies.Biology · 2024Review
- NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders.Progress in neurobiology · 2023Review
- Etiology matters: genetic and acquired prion diseases engage different mechanisms at a presymptomatic stage.Neural regeneration research · 2023Article
- Untangling Tau: Molecular Insights into Neuroinflammation, Pathophysiology, and Emerging Immunotherapies.Current issues in molecular biology · 2023Review
- Tubulin Cytoskeleton in Neurodegenerative Diseases-not Only Primary Tubulinopathies.Cellular and molecular neurobiology · 2023Review
- The Vascular-Immune Hypothesis of Alzheimer's Disease.Biomedicines · 2023Review
- The γ-Adducin 1-357 fragment promotes tau pathology.Frontiers in aging neuroscience · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Sporadic Alzheimer's Disease (AD) is the most common form of dementia, and its severity is characterized by the progressive formation of tau neurofibrillary tangles along a well-described path through the brain. This spatial progression provides the basis for Braak staging of the pathological progression for AD. Tau protein is a necessary component of AD pathology, and recent studies have found that soluble tau species with selectively, but not extensively, modified epitopes accumulate along the path of disease progression before AD-associated insoluble aggregates form. As such, modified tau may represent a key cellular stressing agent that potentiates selective vulnerability in susceptible neurons during AD progression. Specifically, studies have found that tau phosphorylated at sites such as T181, T231, and S396 may initiate early pathological changes in tau by disrupting proper tau localization, initiating tau oligomerization, and facilitating tau accumulation and extracellular export. Thus, this review elucidates potential mechanisms through which tau post-translational modifications (PTMs) may simultaneously serve as key modulators of the spatial progression observed in AD development and as key instigators of early pathology related to neurodegeneration-relevant cellular dysfunctions.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.