Evidence map›Paper›PMID 36499498›Full record

SynthesisInternational journal of molecular sciences2022

Systematic Review of Clinical and Pathophysiological Features of Genetic Creutzfeldt-Jakob Disease Caused by a Val-to-Ile Mutation at Codon 180 in the Prion Protein Gene.

Taiki Matsubayashi, Nobuo Sanjo

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in International journal of molecular sciences, 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
0.4field-weighted citation impact, top 40% 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, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. 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

2 authors at 1 institution in 1 country.

Taiki MatsubayashiDepartment of Neurology and Neurological Science, Tokyo Medical and Dental University Graduate School of Medical and Dental Sciences, 1-5-45 Yushima Bunkyo-ku, Tokyo 113-8510, Japan.
Nobuo SanjoDepartment of Neurology and Neurological Science, Tokyo Medical and Dental University Graduate School of Medical and Dental Sciences, 1-5-45 Yushima Bunkyo-ku, Tokyo 113-8510, Japan.
Tokyo Medical and Dental University · JP

Funding

Grant-in-Aid from the Research Committee of Prion Disease and Slow Virus Infection of the Ministry of Health, Labour, and Welfare of Japan 20FC1054Grant-in-Aid from the Research Committee of Surveillance and Infection Control of Prion Disease of the Ministry of Health, Labour, and Welfare of Japan 20FC2001
6 · The paper itself

Abstract

Genetic Creutzfeldt-Jakob disease (gCJD) is a subtype of genetic prion diseases (gPrDs) caused by the accumulation of mutated pathological prion proteins (PrP

Indexed as

Creutzfeldt-Jakob SyndromePrionsCodonEncephalopathy, Bovine SpongiformHumansMutationPrion ProteinsCodonPrion ProteinsPrionsgenetic Creutzfeldt–Jakob diseasegenetic prion diseasenormal prion proteinspathological prion proteinsprion protein geneV180IVal-to-Ile substitution at codon 180

Identifiers

PMID36499498
PMCPMC9737045
OpenAlexW4311514640

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.