ReviewFrontiers in aging neuroscience2017
Tau Oligomers: Cytotoxicity, Propagation, and Mitochondrial Damage.
Review in Frontiers in aging neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 195 papers, 1 of them a synthesis that pooled it.
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
195 citing papers in PubMed, 1 synthesis or guideline pooled it, 306 citations in OpenAlex.
- Targeting Protein Aggregates with Natural Products: An Optional Strategy for Neurodegenerative Diseases.International journal of molecular sciences · 2023Pooled it
- Temporal Trajectories of the Tau Aggregate Interactome Reveal Stage-Specific Vulnerabilities in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Tau Aggregate Imaging and Transcriptomics of Alzheimer's Disease Brain at Different Stages of Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Emerging Trends and Hot Spots in Tauopathy Research (2003-2025): A Bibliometric Analysis.Brain and behavior · 2026Article
- The Interactions of Tau, RNA, and Stress Granules in Neurodegenerative Disease: A Comprehensive Review.Cells · 2026Review
- A Virus-Like-Particle-Based Conjugate Vaccine Targeting the Microtubule Binding Region of Tau Protein.ACS omega · 2026Article
- 0N4R Tau aggregates producing morphologically different and structurally similar "on-path" and "off-path" oligomers.Chemical communications (Cambridge, England) · 2026Article
- Medial entorhinal-hippocampal desynchronization parallels the emergence of memory impairment in a mouse model of Alzheimer's disease pathology.Cell reports · 2026Article
- FKBP51 inhibition by SAFit2 modulates tau pathology and cognitive deficits in PS19 mice.Alzheimer's research & therapy · 2026Article
- Protopanaxatriol restores cognitive function in okadaic acid-treated mice via direct inhibition of pathological CDK5 activity.Acta pharmacologica Sinica · 2026Article
- TNMD BRICHOS domain attenuates tau pathology and memory deficits in a mouse model of tauopathy.Cell death & disease · 2026Article
- Tau oligomerization induces nuclear lamina invagination and chromatin remodeling in Alzheimer's disease.Acta neuropathologica · 2026Article
- K16F/E22F Mutation Promotes Oligomerization and Alters β-Sheet Topology of Aβ16-22 Peptides: Insights from Molecular Dynamics Simulations.ACS chemical neuroscience · 2026Article
- Toxic mechanisms of amyloid oligomers and therapeutic strategies.Protein science : a publication of the Protein Society · 2026Review
- Tau oligomers modulate synapse fate by eliciting progressive bipartite synapse dysregulation and synapse loss.Molecular neurodegeneration · 2026Article
- Morphological and Hyperphosphorylation Transitions of Nanoscale Tau Aggregates in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-Oligomer Characterization of Tau Phosphorylation and Mechanical State.ACS measurement science au · 2025Article
- Oxidative Stress in DNA Damage and Neurodegenerative Diseases: Unveiling The Mechanisms and Therapeutic Opportunities.Cell biochemistry and biophysics · 2025Review
- APOE isoform-associated tau oligomer polymorphs differ in synaptotoxicity and seeding activity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- PP2A methylesterase, PME-1, and PP2A methyltransferase, LCMT-1, control sensitivity to impairments caused by injury-related oligomeric tau.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
135 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging has long been considered as the main risk factor for several neurodegenerative disorders including a large group of diseases known as tauopathies. Even though neurofibrillary tangles (NFTs) have been examined as the main histopathological hallmark, they do not seem to play a role as the toxic entities leading to disease. Recent studies suggest that an intermediate form of tau, prior to NFT formation, the tau oligomer, is the true toxic species. However, the mechanisms by which tau oligomers trigger neurodegeneration remain unknown. This review summarizes recent findings regarding the role of tau oligomers in disease, including release from cells, propagation from affected to unaffected brain regions, uptake into cells, and toxicity via mitochondrial dysfunction. A greater understanding of tauopathies may lead to future advancements in regards to prevention and treatment.
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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.