Evidence map›Paper›PMID 39559883›Full record

ArticleThe journal of prevention of Alzheimer's disease2024

Quantifying Personalized Shift-Work Molecular Portraits Underlying Alzheimer's Disease through Computational Biology.

Y Xu, G Zhang, L Yang, H Qin, Z Zhou, Q Li, H Liu, R Wang, Z Cai, L Jing and 8 more

Abstract read
In one paragraph

Article in The journal of prevention of Alzheimer's disease, 2024. 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
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.

  1. Review
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

18 authors.

Y XuYanjie Jia, Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China. Email: Jiayanjie1971@zzu.edu.cn; Tao Peng, Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China. Email: pengtao2022@126.com.
G Zhang
L Yang
H Qin
Z Zhou
Q Li
H Liu
R Wang
Z Cai
L Jing
Y Li
Y Yao
Z Gong
P Yuan
T Fu
X Zhao
T Peng
Y Jia

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundShift work, the proven circadian rhythm-disrupting behavior, has been linked to the increased risk of Alzheimer's disease (AD). However, the putative causal effect and potential mechanisms of shift work for AD were still unclear.

methodsMendelian randomization (MR) analysis was performed to discover the putative causal effect of shift work for AD. Expression quantitative trait loci (eQTLs) and transcriptome data were integrated to identify genes causally associated with AD from circadian-related genes. An in vitro experiment was also conducted to validate the expression of target genes. Based on the identified genes, a novel integrative program and 4,077 samples from 16 microarray datasets were leveraged to assess the extent of circadian rhythm disruption (CRD), defined as the clock deviation level (CDL). FINDINGS/

resultsShift work causally increased the risk of AD [odds ratio (OR) = 2.49, 95% CI = 1.79 - 3.19, p = 0.01]. Seven circadian-related genes were causally associated with AD, including CCS, CDS2, MYRIP, NRP1, PLEKHA5, POLR1D, and PPP4C. These genes were significantly correlated with the circadian rhythm pathway. CDL was higher in CRD mice group, shift work group, sleep restriction group, and AD patients compared to control mice group (p = 0.043), non-shift group (p = 0.004), sleep extension group (p = 0.025), and health controls (multiple cohorts, p < 0.05). Additionally, CDL was also significantly correlated with AD's clinical biomarkers. INTERPRETATIONS/

conclusionBy combining GWAS and transcriptome data, this study demonstrated the causal role of CRD behavior in AD, identified the potential target genes in shift work-induced AD, and generated CDL to characterize CRD status, which provided evidence and prospects for disease prevention and future therapeutic interventions.

Indexed as

Alzheimer DiseaseComputational BiologyMendelian Randomization AnalysisAnimalsCircadian RhythmHumansMaleMiceQuantitative Trait LociShift Work ScheduleTranscriptomeAlzheimer’s diseaseCircadian rhythmgeneticsgenome-wide association studyshift work

Identifiers

PMID39559883
PMCPMC11573866

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.