ReviewFrontiers in cellular neuroscience2019
Altered Levels and Isoforms of Tau and Nuclear Membrane Invaginations in Huntington's Disease.
Review in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Stage-dependent tau-PET signatures in Huntington's disease revealed by [¹⁸F]PI-2620.European journal of nuclear medicine and molecular imaging · 2026Article
- Tau levels in platelets isolated from Huntington's disease patients serve as a biomarker of disease severity.Journal of neurology · 2025Article
- Role of Tau Protein in Neurodegenerative Diseases and Development of Its Targeted Drugs: A Literature Review.Molecules (Basel, Switzerland) · 2024Review
- Cognitive phenotype and neurodegeneration associated with Tau in Huntington's disease.Annals of clinical and translational neurology · 2024Article
- Tau Protein Alterations Induced by Hypobaric Hypoxia Exposure.International journal of molecular sciences · 2024Review
- Tau: a biomarker of Huntington's disease.Molecular psychiatry · 2023Review
- The Emerging Landscape of Natural Small-molecule Therapeutics for Huntington's Disease.Current neuropharmacology · 2023Review
- Age-Dependent Increase in Tau Phosphorylation at Serine 396 in Huntington's Disease Prefrontal Cortex.Journal of Huntington's disease · 2023Article
- Implications of Tau Dysregulation in Huntington's Disease and Potential for New Therapeutics.Journal of Huntington's disease · 2023Review
- Untangling the Role of Tau in Huntington's Disease Pathology.Journal of Huntington's disease · 2023Review
- Nuclear import receptors are recruited by FG-nucleoporins to rescue hallmarks of TDP-43 proteinopathy.Molecular neurodegeneration · 2022Article
- Review
- Phosphorylated Tau in Alzheimer's Disease and Other Tauopathies.International journal of molecular sciences · 2022Review
- Mechanics and functional consequences of nuclear deformations.Nature reviews. Molecular cell biology · 2022Review
- A Glimpse of Molecular Biomarkers in Huntington's Disease.International journal of molecular sciences · 2022Review
- High altitude is associated with pTau deposition, neuroinflammation, and myelin loss.Scientific reports · 2022Article
- Altered nuclear architecture in blood cells from Huntington's disease patients.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Article
- Non-Canonical Roles of Tau and Their Contribution to Synaptic Dysfunction.International journal of molecular sciences · 2021Review
- Gene targeting techniques for Huntington's disease.Ageing research reviews · 2021Review
- An unusual presentation of Huntington's disease.Clinical case reports · 2021Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since the early reports of neurofibrillary Tau pathology in brains of some Huntington's disease (HD) patients, mounting evidence of multiple alterations of Tau in HD brain tissue has emerged in recent years. Such Tau alterations range from increased total levels, imbalance of isoforms generated by alternative splicing (increased 4R-/3R-Tau ratio) or by post-translational modifications such as hyperphosphorylation or truncation. Besides, the detection in HD brains of a new Tau histopathological hallmark known as Tau nuclear rods (TNRs) or Tau-positive nuclear indentations (TNIs) led to propose HD as a secondary Tauopathy. After their discovery in HD brains, TNIs have also been reported in hippocampal neurons of early Braak stage AD cases and in frontal and temporal cortical neurons of FTD-MAPT cases due to the intronic IVS10+16 mutation in the Tau gene (MAPT) which results in an increased 4R-/3R-Tau ratio similar to that observed in HD. TNIs are likely pathogenic for contributing to the disturbed nucleocytoplasmic transport observed in HD. A key question is whether correction of any of the mentioned Tau alterations might have positive therapeutic implications for HD. The beneficial effect of decreasing Tau expression in HD mouse models clearly implicates Tau in HD pathogenesis. Such beneficial effect might be exerted by diminishing the excess total levels of Tau or specifically by diminishing the excess 4R-Tau, as well as any of their downstream effects. In any case, since gene silencing drugs are under development to attenuate both Huntingtin (HTT) expression for HD and MAPT expression for FTD-MAPT, it is conceivable that the combined therapy in HD patients might be more effective than HTT silencing alone.
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