Evidence map›Paper›PMID 35379479›Full record

ArticleTrends in neurosciences2022

Fatty acid balance regulates α-synuclein pathology.

Stav Cohen-Adiv, Avraham Ashkenazi

Abstract readComment
PubMed Publisher
In one paragraph

Article in Trends in neurosciences, 2022. 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
0.4field-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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Cellular fibronectin exacerbates α-synuclein aggregation via integrin alpha4beta1 mediated PARP1 and SCD elevation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Stav Cohen-AdivDepartment of Cell and Developmental Biology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Avraham AshkenaziDepartment of Cell and Developmental Biology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. Electronic address: ashkenaziavi@tauex.tau.ac.il.
Tel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A recent study by Tripathi et al. used a protein engineering approach to demonstrate that cellular stress caused by familial α-synuclein mutations can be alleviated by altering the monounsaturated fatty acid equilibrium in neuronal cells. This work supports the notion that metabolic perturbation of lipids may be involved in the pathogenesis of Parkinson's disease.

Indexed as

alpha-SynucleinParkinson DiseaseFatty AcidsHumansMutationalpha-SynucleinFatty Acidsaggregation-prone proteinscellular membranemonounsaturated fatty acidParkinson's diseaseα-synuclein

Identifiers

PMID35379479
OpenAlexW4223974361

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.