Evidence map›Paper›PMID 36476347›Full record

ArticleActa neuropathologica communications2022

Spinocerebellar ataxia type 17-digenic TBP/STUB1 disease: neuropathologic features of an autopsied patient.

Rie Saito, Yui Tada, Daisuke Oikawa, Yusuke Sato, Makiko Seto, Akira Satoh, Kodai Kume, Nozomi Ueki, Masahiro Nakashima, Shintaro Hayashi and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

5 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Movement Disorders in Hereditary Cerebellar Ataxia.Movement disorders clinical practice · 2025
    Article
  3. Article
  4. Article
  5. GDF9Cell communication and signaling : CCS · 2024
    Article
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

14 authors at 7 institutions in 1 country.

Rie SaitoDepartments of Pathology, Brain Research Institute, Niigata University, 1-757 Asahimachi, Chuo-ku, Niigata, 951-8585, Japan.
Yui TadaDepartment of Molecular Epidemiology, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8553, Japan.
Daisuke OikawaDepartment of Medical Biochemistry, Graduate School of Medicine, Osaka Metropolitan University, 1- 4-3 Asahi-machi, Abeno-ku, Osaka, 545-8585, Japan.
Yusuke SatoDepartment of Chemistry and Biotechnology, Graduate School of Engineering, Tottori University, 4-101 Koyama-cho Minami, Tottori, 680-8552, Japan.
Makiko SetoSection of Neurology, Nagasaki Kita Hospital, 800 Motomurago, Togitsu-cho, Nishisonogi-gun, Nagasaki, 851-2103, Japan.
Akira SatohSection of Neurology, Nagasaki Kita Hospital, 800 Motomurago, Togitsu-cho, Nishisonogi-gun, Nagasaki, 851-2103, Japan.
Kodai KumeDepartment of Molecular Epidemiology, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8553, Japan.
Nozomi UekiDepartment of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki, 852-8523, Japan.
Masahiro NakashimaDepartment of Tumor and Diagnostic Pathology, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki, 852-8523, Japan.
Shintaro HayashiDepartments of Pathology, Brain Research Institute, Niigata University, 1-757 Asahimachi, Chuo-ku, Niigata, 951-8585, Japan.
Yasuko ToyoshimaDepartments of Pathology, Brain Research Institute, Niigata University, 1-757 Asahimachi, Chuo-ku, Niigata, 951-8585, Japan.
Fuminori TokunagaDepartment of Medical Biochemistry, Graduate School of Medicine, Osaka Metropolitan University, 1- 4-3 Asahi-machi, Abeno-ku, Osaka, 545-8585, Japan.
Hideshi KawakamiDepartment of Molecular Epidemiology, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8553, Japan.
Akiyoshi KakitaDepartments of Pathology, Brain Research Institute, Niigata University, 1-757 Asahimachi, Chuo-ku, Niigata, 951-8585, Japan. kakita@bri.niigata-u.ac.jp.
Hiroshima University · JPNiigata University · JPNagasaki Ajisai Hospital · JPNagasaki University · JPOsaka Metropolitan UniversityNagashima Hospital · JPTottori University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spinocerebellar ataxia (SCA) type 17-digenic TBP/STUB1 disease (SCA17-DI) has been recently segregated from SCA17, caused by digenic inheritance of two gene mutations - intermediate polyglutamine-encoding CAG/CAA repeat expansions (polyQ) in TBP (TBP

Indexed as

Huntington DiseaseSpinocerebellar AtaxiasAutopsyHumansNeuropathologyUbiquitin-Protein LigasesSTUB1 protein, humanUbiquitin-Protein LigasesHuntington’s disease-like symptomsNeuropathologypolyQ stretchSCA17-DISTUB1TBP

Identifiers

PMID36476347
PMCPMC9727856
OpenAlexW4311572755

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.