Evidence map›Paper›PMID 31861888›Full record

ArticleBrain sciences2019

Colocalization of BRCA1 with Tau Aggregates in Human Tauopathies.

Masanori Kurihara, Tatsuo Mano, Yuko Saito, Shigeo Murayama, Tatsushi Toda, Atsushi Iwata

Open access · goldAbstract read
In one paragraph

Article in Brain sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Assessing the Clinical Relevance ofCurrent oncology (Toronto, Ont.) · 2026
    Article
  3. Review
  4. Article
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  6. Targeting Endogenous Tau in Seeded Tauopathy Models Inhibits Tau Spread.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
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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

6 authors at 4 institutions in 1 country.

Masanori KuriharaDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Tatsuo ManoDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Yuko SaitoDepartment of Pathology and Laboratory Medicine, National Center Hospital, National Center of Neurology and Psychiatry, Tokyo 187-8551, Japan.
Shigeo MurayamaDepartment of Neurology and Neuropathology (the Brain Bank for Aging Research), Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology, Tokyo 173-0015, Japan.
Tatsushi TodaDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Atsushi IwataDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
The University of Tokyo · JPJapan Society for the Promotion of Science · JPNational Center of Neurology and Psychiatry · JPTokyo Metropolitan Geriatric Hospital · JP

Funding

Japan Agency for Medical Research and Development JP18dm0107069Japan Agency for Medical Research and Development JP18dm0107103Japan Society for the Promotion of Science JP16H05319Japan Society for the Promotion of Science JP16H06277Japan Society for the Promotion of Science JP19J10924Japan Society for the Promotion of Science JP19K17027National Center of Neurology and Psychiatry 30-8
6 · The paper itself

Abstract

The mechanism of neuronal dysfunction via tau aggregation in tauopathy patients is controversial. In Alzheimer's disease (AD), we previously reported mislocalization of the DNA repair nuclear protein BRCA1, its coaggregation with tau, and the possible importance of the subsequent DNA repair dysfunction. However, whether this dysfunction in BRCA1 also occurs in other tauopathies is unknown. The aim of this study was to evaluate whether BRCA1 colocalizes with tau aggregates in the cytoplasm in the brains of the patients with tauopathy. We evaluated four AD, two Pick's disease (PiD), three progressive supranuclear palsy (PSP), three corticobasal degeneration (CBD), four normal control, and four disease control autopsy brains. Immunohistochemistry was performed using antibodies against BRCA1 and phosphorylated tau (AT8). Colocalization was confirmed by immunofluorescence double staining. Colocalization of BRCA1 with tau aggregates was observed in neurofibrillary tangles and neuropil threads in AD, pick bodies in PiD, and globose neurofibrillary tangles and glial coiled bodies in PSP. However, only partial colocalization was observed in tuft-shaped astrocytes in PSP, and no colocalization was observed in CBD. Mislocalization of BRCA1 was not observed in disease controls. BRCA1 was mislocalized to the cytoplasm and colocalized with tau aggregates in not only AD but also in PiD and PSP. Mislocalization of BRCA1 by tau aggregates may be involved in the pathogenesis of PiD and PSP.

Indexed as

Alzheimer’s diseaseBRCA1corticobasal degenerationDNA repairPick’s diseaseprogressive supranuclear palsyprotein aggregationtau

Identifiers

PMID31861888
PMCPMC7016802
OpenAlexW2996353551

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.