Evidence map›Paper›PMID 37639066›Full record

ArticleMolecular neurobiology2024

Abnormal Brain Protein Abundance and Cross-tissue mRNA Expression in Amyotrophic Lateral Sclerosis.

Yanni Ma, Tingting Jia, Fengqin Qin, Yongji He, Feng Han, Chengcheng Zhang

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

Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

6 authors at 4 institutions in 1 country.

Yanni MaMental Health Center and Psychiatric Laboratory, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, 610041, Sichuan, China.
Tingting JiaMental Health Center and Psychiatric Laboratory, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, 610041, Sichuan, China.
Fengqin QinDepartment of Neurology, The 3Rd Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, China.
Yongji HeClinical Trial Center, National Medical Products Administration Key Laboratory for Clinical Research and Evaluation of Innovative Drugs, West China Hospital Sichuan University, Chengdu, People's Republic of China.
Feng HanDepartment of Emergency Medicine, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, China.
Chengcheng ZhangMental Health Center and Psychiatric Laboratory, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, 610041, Sichuan, China. zhangcc89@foxmail.com.ORCID http://orcid.org/0000-0002-2992-6291
Sichuan University · CNChengdu Medical College · CNHainan General Hospital · CNNational Medical Products Administration · CN

Funding

College Students' innovation and entrepreneurship training program 20221174LKey R & D Projects of Science and Technology Department of Sichuan Province 2021YFS0248Postdoctoral Foundation of West China Hospital 2020HXBH163
6 · The paper itself

Abstract

Due to the limitations of the present risk genes in understanding the etiology of amyotrophic lateral sclerosis (ALS), it is necessary to find additional causative genes utilizing novel approaches. In this study, we conducted a two-stage proteome-wide association study (PWAS) using ALS genome-wide association study (GWAS) data (N = 152,268) and two distinct human brain protein quantitative trait loci (pQTL) datasets (ROSMAP N = 376 and Banner N = 152) to identify ALS risk genes and prioritized candidate genes with Mendelian randomization (MR) and Bayesian colocalization analysis. Next, we verified the aberrant expression of risk genes in multiple tissues, including lower motor neurons, skeletal muscle, and whole blood. Six ALS risk genes (SCFD1, SARM1, TMEM175, BCS1L, WIPI2, and DHRS11) were found during the PWAS discovery phase, and SARM1 and BCS1L were confirmed during the validation phase. The following MR (p = 2.10 × 10

Indexed as

Amyotrophic Lateral Sclerosis17-Hydroxysteroid DehydrogenasesATPases Associated with Diverse Cellular ActivitiesBayes TheoremBrainElectron Transport Complex IIIGenome-Wide Association StudyHumansProteomeRNA, Messenger17-Hydroxysteroid DehydrogenasesATPases Associated with Diverse Cellular ActivitiesBCS1L protein, humanDHRS11 protein, humanElectron Transport Complex IIIProteomeRNA, MessengerAmyotrophic lateral sclerosis (ALS)Differential expression analysisProtein quantitative trait loci (pQTL)Proteome-wide association study

Identifiers

PMID37639066
PMCPMC10791788
OpenAlexW4386208961

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Registered trials

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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.