ArticleFrontiers in aging neuroscience2018
Relevance of Phosphorylation and Truncation of Tau to the Etiopathogenesis of Alzheimer's Disease.
Article in Frontiers in aging neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 121 citations in OpenAlex.
- MAPT-derived circTau6 induces tau pathogenesis and neurodegeneration by encoding Tau variants.Molecular psychiatry · 2026Article
- Tau seeds induce neurofibrillary tangle formation across brain regions via individual-specific connectivity.Neuron · 2026Article
- Evaluation of CSF and plasma tau species as fluid surrogate candidates for tau PET in prodromal to moderate Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- N-terminally acetylated Met11-Tau: a new pathological truncated Tau species with functional relevance in Alzheimer's disease.Translational neurodegeneration · 2026Article
- Autophagy Activators Normalize Aberrant Tau Proteostasis and Rescue Synapses in Human Familial Alzheimer's Disease iPSC-Derived Cortical Organoids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Lysine methylation is an endogenous post-translational modifications of tau protein in human brain and a modulator of aggregation propensity.Methods in enzymology · 2026Article
- Safety, tolerability and biomarker results of bepranemab in participants with progressive supranuclear palsy: a randomised, multicentre, double-blind, placebo-controlled, phase 1b trial.BMJ neurology open · 2026Article
- From seeds to symptoms: the molecular landscape of tau seeding in Alzheimer's disease.Frontiers in neuroscience · 2026Review
- Hypothesis-Driven Insights and Clinical Trial Updates in Alzheimer's Disease Pathogenesis.CNS & neurological disorders drug targets · 2026Review
- Is the Era of One-Size-Fits-All Alzheimer's Treatment Officially Over?Journal of molecular neuroscience : MN · 2025Review
- New Approach for Targeting Small-Molecule Candidates for Intrinsically Disordered Proteins.Methods and protocols · 2025Article
- Formaldehyde induces and promotes Alzheimer's disease pathologies in a 3D human neural cell culture model.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2025Article
- Glycogen synthase kinase-3: the master switch driving neurodegeneration in Alzheimer's disease and Parkinson's disease.Archives of toxicology · 2025Review
- Alzheimer's disease patient brain extracts induce multiple pathologies in novel vascularized neuroimmune organoids for disease modeling and drug discovery.Molecular psychiatry · 2025Article
- The Proteoform Landscape of Tau from the Human Brain.Journal of proteome research · 2025Article
- Precision Medicine in Neurodegenerative Diseases: Genomic Approaches to Target Amyloid-β, Tau, and Alpha-Synuclein Pathways.Current genomics · 2025Review
- Tau accumulation is cleared by the induced expression of VCP via autophagy.Acta neuropathologica · 2024Article
- Proteolysis of tau by granzyme A in tauopathies generates fragments that are aggregation prone.The Biochemical journal · 2024Article
- Posttreatment with PaPE-1 Protects from Aβ-Induced Neurodegeneration Through Inhibiting the Expression of Alzheimer's Disease-Related Genes and Apoptosis Process That Involves Enhanced DNA Methylation of Specific Genes.Molecular neurobiology · 2024Article
- Endogenous tau released from humanbioRxiv : the preprint server for biology · 2024Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microtubule (MT) associated protein tau is abnormally hyperphosphorylated and aggregated into paired helical filaments (PHFs), which manifest as neurofibrillary tangles (NFTs) in the brains of individuals with Alzheimer's disease (AD) and related tauopathies. Hyperphosphorylation and truncation of tau have been linked to the progression of the disease. However, the nature of phosphorylation and truncation of tau in AD brain are not very clear. In the present study we investigated the association of phosphorylation and truncation with high-molecular weight oligomers of tau (HMW-tau) in post-mortem AD brain by western blots. We found that tau from AD brain appears as a smear from low molecular weight (LMW) to HMW tau species in western blots developed with pan-tau antibodies. Similar level of LMW-tau was found in AD and control brains, whereas HMW-tau was found in AD brain only. HMW-tau was hyperphosphorylated at multiple sites and not unphosphorylated at Ser46 or Ser198/199/202. HMW-tau was weakly labeled by tau antibodies 43D against a.a. 6-18 and HT7 against a.a. 159-163 of tau, whereas, the C-terminal antibodies, tau46 and tau46.1, strongly labeled HMW-tau. The ratio of HMW-tau/LMW-tau detected by tau antibodies increased as the epitope of the tau antibodies ranges from N-terminal to C-terminal. The level of tau truncated at Asp421 was increased in AD brain, but was poorly associated with the HMW-tau. These findings suggest that tau pathogenesis involves both hyperphosphorylation and dominantly N-terminal truncation of tau in AD.
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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.