ArticleJournal of Alzheimer's disease : JAD2021
Molecular Processing of Tau Protein in Progressive Supranuclear Palsy: Neuronal and Glial Degeneration.
Article in Journal of Alzheimer's disease : JAD, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Cerebrospinal fluid biomarkers for diagnosis of Parkinson's disease: a systematic review and network meta-analysis.Journal of neurology · 2025Pooled it
- The role of SUMOylation in regulating proteins that drive neuronal disease progression.Biochemistry and biophysics reports · 2026Review
- Context-dependent toxicity of human tau isoforms in a Drosophila tauopathy model.Biology open · 2026Article
- Article
- A Mathematical Model of Cellular Aggregation Predicts Patterns of Tau Accumulation in Neurodegenerative Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Tau-Mitochondria Interactions in Neurodegeneration: Mechanisms and Therapeutic Potential.Cellular and molecular neurobiology · 2025Review
- Brain Networks Route Neurodegeneration Patterns in Patients with Progressive Supranuclear Palsy.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- A novel pThr217 tau monoclonal antibody reveals neuropathological heterogeneity in tauopathies.Scientific reports · 2025Article
- Differences in the soluble and insoluble proteome between primary tauopathies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The Role of Tau in Neuronal Function and Neurodegeneration.Neurology international · 2025Review
- Modeling Sporadic Progressive Supranuclear Palsy in 3D Midbrain Organoids: Recapitulating Disease Features for In Vitro Diagnosis and Drug Discovery.Annals of neurology · 2025Article
- Serum Tau Species in Progressive Supranuclear Palsy: A Pilot Study.Diagnostics (Basel, Switzerland) · 2024Article
- Misfolding and aggregation in neurodegenerative diseases: protein quality control machinery as potential therapeutic clearance pathways.Cell communication and signaling : CCS · 2024Review
- The Role of Liquid-Liquid Phase Separation in the Accumulation of Pathological Proteins: New Perspectives on the Mechanism of Neurodegenerative Diseases.Aging and disease · 2024Review
- Alzheimer's Disease Puzzle: Delving into Pathogenesis Hypotheses.Aging and disease · 2024Review
- Insights into amyloid precursor protein target through PPI network analysis.Bioinformation · 2024Article
- Tolfenamic Acid Derivatives: A New Class of Transcriptional Modulators with Potential Therapeutic Applications for Alzheimer's Disease and Related Disorders.International journal of molecular sciences · 2023Article
- Concomitant Neuronal Tau Deposition and FKBP52 Decrease Is an Early Feature of Different Human and Experimental Tauopathies.Journal of Alzheimer's disease : JAD · 2023Article
- Interpretable Classification of Tauopathies with a Convolutional Neural Network Pipeline Using Transfer Learning and Validation against Post-Mortem Clinical Cases of Alzheimer's Disease and Progressive Supranuclear Palsy.Current issues in molecular biology · 2022Article
- Tau interactome and RNA binding proteins in neurodegenerative diseases.Molecular neurodegeneration · 2022Review
Corrections and comments
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Authors and funding
16 authors at 8 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlzheimer's disease (AD) and progressive supranuclear palsy (PSP) are examples of neurodegenerative diseases, characterized by abnormal tau inclusions, that are called tauopathies. AD is characterized by highly insoluble paired helical filaments (PHFs) composed of tau with abnormal post-translational modifications. PSP is a neurodegenerative disease with pathological and clinical heterogeneity. There are six tau isoforms expressed in the adult human brain, with repeated microtubule-binding domains of three (3R) or four (4R) repeats. In AD, the 4R:3R ratio is 1:1. In PSP, the 4R isoform predominates. The lesions in PSP brains contain phosphorylated tau aggregates in both neurons and glial cells.
objectiveOur objective was to evaluate and compare the processing of pathological tau in PSP and AD.
methodsDouble and triple immunofluorescent labeling with antibodies to specific post-translational tau modifications (phosphorylation, truncation, and conformational changes) and thiazin red (TR) staining were carried out and analyzed by confocal microscopy.
resultsOur results showed that PSP was characterized by phosphorylated tau in neurofibrillary tangles (NFTs) and glial cells. Tau truncated at either Glu391 or Asp421 was not observed. Extracellular NFTs (eNFTs) and glial cells in PSP exhibited a strong affinity for TR in the absence of intact or phosphorylated tau.
conclusionPhosphorylated tau was as abundant in PSP as in AD. The development of eNFTs from both glial cells and neuronal bodies suggests that truncated tau species, different from those observed in AD, could be present in PSP. Additional studies on truncated tau within PSP lesions could improve our understanding of the pathological processing of tau and help identify a discriminatory biomarker for AD and PSP.
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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.