Evidence map›Paper›PMID 30573872›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2019

Spectrum of tau pathologies in Huntington's disease.

Swikrity Upadhyay Baskota, Oscar L Lopez, J Timothy Greenamyre, Julia Kofler

Open access · bronzeAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Stage-dependent tau-PET signatures in Huntington's disease revealed by [¹⁸F]PI-2620.European journal of nuclear medicine and molecular imaging · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Tau Protein Alterations Induced by Hypobaric Hypoxia Exposure.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Tau: a biomarker of Huntington's disease.Molecular psychiatry · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. Classification of diseases with accumulation of Tau protein.Neuropathology and applied neurobiology · 2022
    Article
  15. Review
  16. Review
  17. Editorial: Tau Protein: Mechanisms From Health to Degeneration.Frontiers in molecular neuroscience · 2021
    Article
  18. Review
  19. Review
  20. Huntington disease: Advances in the understanding of its mechanisms.Clinical parkinsonism & related disorders · 2020
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Swikrity Upadhyay BaskotaDepartment of Pathology, University of Pittsburgh, Pittsburgh, PA, USA.
Oscar L LopezDepartment of Neurology, University of Pittsburgh, Pittsburgh, PA, USA.
J Timothy GreenamyreDepartment of Neurology, University of Pittsburgh, Pittsburgh, PA, USA.
Julia KoflerDepartment of Pathology, University of Pittsburgh, Pittsburgh, PA, USA. koflerjk@upmc.edu.
University of Pittsburgh · USInstitute for Neurodegenerative Disorders · US

Funding

TREATMENT OF DEPRESSION IN ALZHEIMER'S DISEASEP50AG005133 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BECKER, JAMES T. · 1985 to 2019
$43.0M
Synaptic Resilience to Psychosis in Alzheimer DiseaseR01MH116046 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Julia K Kofler, ROBERT A SWEET · 2018 to 2026
$6.6M
NIA NIH HHS P50 AG005133NIMH NIH HHS R01 MH116046
6 · The paper itself

Abstract

Huntington's disease (HD) is an autosomal dominant disorder caused by a trinucleotide expansion in the huntingtin gene. Recently, a new role for tau has been implicated in the pathogenesis of HD, whereas others have argued that postmortem tau pathology findings are attributable to concurrent Alzheimer's disease pathology. The frequency of other well-defined common age-related tau pathologies in HD has not been examined in detail. In this single center, retrospective analysis, we screened seven cases of Huntington's disease (5 females, 2 males, age at death: 47-73 years) for neuronal and glial tau pathology using phospho-tau immunohistochemistry. All seven cases showed presence of neuronal tau pathology. Five cases met diagnostic criteria for primary age-related tauopathy (PART), with three cases classified as definite PART and two cases as possible PART, all with a Braak stage of I. One case was diagnosed with low level of Alzheimer's disease neuropathologic change. In the youngest case, rare perivascular aggregates of tau-positive neurons, astrocytes and processes were identified at sulcal depths, meeting current neuropathological criteria for stage 1 chronic traumatic encephalopathy (CTE). Although the patient had no history of playing contact sports, he experienced several falls, but no definitive concussions during his disease course. Three of the PART cases and the CTE-like case showed additional evidence of aging-related tau astrogliopathy. None of the cases showed significant tau pathology in the striatum. In conclusion, while we found evidence for tau hyperphosphorylation and aggregation in all seven of our HD cases, the tau pathology was readily classifiable into known diagnostic entities and most likely represents non-specific age- or perhaps trauma-related changes. As the tau pathology was very mild in all cases and not unexpected for a population of this age range, it does not appear that the underlying HD may have promoted or accelerated tau accumulation.

Indexed as

AgedAge FactorsAlzheimer DiseaseBrainFemaleHumansHuntington DiseaseImmunohistochemistryMaleMiddle AgedNeuronsPhosphorylationRetrospective StudiesTauopathiestau Proteinstau Proteins

Identifiers

PMID30573872
PMCPMC9342691
OpenAlexW2905232989

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.