ArticleFrontiers in neurology2013
Hyperphosphorylation-induced tau oligomers.
Article in Frontiers in neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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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.
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Who cites it
48 citing papers in PubMed, 112 citations in OpenAlex.
- The Role and Molecular Mechanism of Icaritin in the Treatment of Alzheimer's Disease.Current medicinal chemistry · 2026Review
- Thymoquinone-Loaded Hexosomal Nanoparticles Attenuate Neuroinflammation and Improve Cognitive Function in an Alzheimer's Disease Mouse Model.International journal of nanomedicine · 2026Article
- Marmosets as model systems for the study of Alzheimer's disease and related dementias: Substantiation of physiological tau 3R and 4R isoform expression and phosphorylation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Integrated Gut Microbiota, Metabolomics, and Network Pharmacology to Investigate the Anti-Alzheimer's Mechanism of Tripterygium Glycoside.Neuropsychiatric disease and treatment · 2025Article
- Glucose Metabolic Abnormality: A Crosstalk between Depression and Alzheimer's Disease.Current neuropharmacology · 2025Review
- Trioxidized cysteine in the aging proteome mimics the structural dynamics and interactome of phosphorylated serine.Aging cell · 2024Article
- Visualization Analysis of Tau Protein in the Brain of Alzheimer's Disease: A Scoping Literature Review.Current Alzheimer research · 2024Article
- Mechanisms of genotoxicity and proteotoxicity induced by the metalloids arsenic and antimony.Cellular and molecular life sciences : CMLS · 2023Review
- Review of Phytochemical Potency as a Natural Anti-Molecules (Basel, Switzerland) · 2023Review
- Alterations in iron content, iron-regulatory proteins and behaviour without tau pathology at one year following repetitive mild traumatic brain injury.Acta neuropathologica communications · 2023Article
- Microglia degrade Tau oligomers deposit via purinergic P2Y12-associated podosome and filopodia formation and induce chemotaxis.Cell & bioscience · 2023Article
- Soluble pathogenic tau enters brain vascular endothelial cells and drives cellular senescence and brain microvascular dysfunction in a mouse model of tauopathy.Nature communications · 2023Article
- Extracellular Tau Oligomers Damage the Axon Initial Segment.Journal of Alzheimer's disease : JAD · 2023Article
- Disease-Modifying Effects of Non-Invasive Electroceuticals on β-Amyloid Plaques and Tau Tangles for Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Transcranial Electromagnetic Treatment Stops Alzheimer's Disease Cognitive Decline over a 2½-Year Period: A Pilot Study.Medicines (Basel, Switzerland) · 2022Article
- Hyperphosphorylated tau self-assembles into amorphous aggregates eliciting TLR4-dependent responses.Nature communications · 2022Article
- Identification of HnRNPC as a novel Tau exon 10 splicing factor using RNA antisense purification mass spectrometry.RNA biology · 2022Article
- Distribution of tau hyperphosphorylation in canine dementia resembles early Alzheimer's disease and other tauopathies.Brain pathology (Zurich, Switzerland) · 2021Article
- Tau Ubiquitination in Alzheimer's Disease.Frontiers in neurology · 2021Review
- The role of wild-type tau in Alzheimer's disease and related tauopathies.Journal of life sciences (Westlake Village, Calif.) · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In normal adult brain the microtubule associated protein (MAP) tau contains 2-3 phosphates per mol of the protein and at this level of phosphorylation it is a soluble cytosolic protein. The normal brain tau interacts with tubulin and promotes its assembly into microtubules and stabilizes these fibrils. In Alzheimer disease (AD) brain tau is three to fourfold hyperphosphorylated. The abnormally hyperphosphorylated tau binds to normal tau instead of the tubulin and this binding leads to the formation of tau oligomers. The tau oligomers can be sedimented at 200,000 × g whereas the normal tau under these conditions remains in the supernatant. The abnormally hyperphosphorylated tau is capable of sequestering not only normal tau but also MAP MAP1 and MAP2 and causing disruption of the microtubule network promoted by these proteins. Unlike Aβ and prion protein (PrP) oligomers, tau oligomerization in AD and related tauopathies is hyperphosphorylation-dependent; in vitro dephosphorylation of AD P-tau with protein phosphatase 2A (PP2A) inhibits and rehyperphosphorylation of the PP2A-AD P-tau with more than one combination of tau protein kinases promotes its oligomerization. In physiological assembly conditions the AD P-tau readily self-assembles into paired helical filaments. Missense tau mutations found in frontotemporal dementia apparently lead to tau oligomerization and neurofibrillary pathology by promoting its abnormal hyperphosphorylation. Dysregulation of the alternative splicing of tau that alters the 1:1 ratio of the 3-repeat: 4-repeat taus such as in Down syndrome, Pick disease, and progressive supranuclear palsy leads to the abnormal hyperphosphorylation of tau.
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