Evidence map›Paper›PMID 38596238›Full record

ReviewOxford open neuroscience2023

Genetic modifiers of synucleinopathies-lessons from experimental models.

Rachel Min Qi Lee, Tong-Wey Koh

Open access · diamondAbstract readReview
In one paragraph

Review in Oxford open neuroscience, 2023. 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
0.8field-weighted citation impact, top 27% 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, 4 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 2 institutions in 1 country.

Rachel Min Qi LeeTemasek Life Sciences Laboratory, 1 Research Link, Singapore, 117604, Singapore.
Tong-Wey KohTemasek Life Sciences Laboratory, 1 Research Link, Singapore, 117604, Singapore.
National University of Singapore · SGTemasek Life Sciences Laboratory · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

α-Synuclein is a pleiotropic protein underlying a group of progressive neurodegenerative diseases, including Parkinson's disease and dementia with Lewy bodies. Together, these are known as synucleinopathies. Like all neurological diseases, understanding of disease mechanisms is hampered by the lack of access to biopsy tissues, precluding a real-time view of disease progression in the human body. This has driven researchers to devise various experimental models ranging from yeast to flies to human brain organoids, aiming to recapitulate aspects of synucleinopathies. Studies of these models have uncovered numerous genetic modifiers of α-synuclein, most of which are evolutionarily conserved. This review discusses what we have learned about disease mechanisms from these modifiers, and ways in which the study of modifiers have supported ongoing efforts to engineer disease-modifying interventions for synucleinopathies.

Indexed as

Drug targetsGenetic modifiersLewy bodiesParkinson’s diseaseSNCAα-synuclein

Identifiers

PMID38596238
PMCPMC10913850
OpenAlexW4323656678

What Socratic 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 Socratic graph.