Evidence map›Paper›PMID 28421536›Full record

ReviewMolecular neurobiology2018

Lysosomal Quality Control in Prion Diseases.

Priyanka Majumder, Oishee Chakrabarti

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 97% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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.

Priyanka MajumderBiophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, Sector-1, Block-AF, Bidhannagar, Kolkata, West Bengal, 700064, India.
Oishee ChakrabartiBiophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, Sector-1, Block-AF, Bidhannagar, Kolkata, West Bengal, 700064, India. oishee.chakrabarti@saha.ac.in.
Saha Institute of Nuclear Physics · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prion diseases are transmissible, familial or sporadic. The prion protein (PrP), a normal cell surface glycoprotein, is ubiquitously expressed throughout the body. While loss of function of PrP does not elicit apparent phenotypes, generation of misfolded forms of the protein or its aberrant metabolic isoforms has been implicated in a number of neurodegenerative disorders such as scrapie, kuru, Creutzfeldt-Jakob disease, fatal familial insomnia, Gerstmann-Sträussler-Scheinker and bovine spongiform encephalopathy. These diseases are all phenotypically characterised by spongiform vacuolation of the adult brain, hence collectively termed as late-onset spongiform neurodegeneration. Misfolded form of PrP (PrP

Indexed as

AnimalsBrainHumansLysosomesPrion DiseasesPrionsQuality ControlSignal TransductionPrionsAutophagosomeESCRT pathwayLysosomePrP

Identifiers

PMID28421536
OpenAlexW2607112089

What OpenQuestion holds

Textmetadata
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.