Evidence map›Paper›PMID 34956428›Full record

ArticleThe EPMA journal2021

Integrative genomic analysis of PPP3R1 in Alzheimer's disease: a potential biomarker for predictive, preventive, and personalized medical approach.

Zhike Zhou, Jun Bai, Shanshan Zhong, Rongwei Zhang, Kexin Kang, Xiaoqian Zhang, Ying Xu, Chuansheng Zhao, Mei Zhao

Open access · greenAbstract read
In one paragraph

Article in The EPMA journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. DNA methylation site loss for plasticity-led novel trait genetic fixation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

9 authors at 3 institutions in 2 countries.

Zhike ZhouDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang 110001 Liaoning, People's Republic of China.
Jun BaiCancer Systems Biology Center, The China-Japan, Union Hospital, Jilin University, Changchun 130033 Jilin, People's Republic of China.
Shanshan ZhongDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang 110001 Liaoning, People's Republic of China.
Rongwei ZhangDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang 110001 Liaoning, People's Republic of China.
Kexin KangDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang 110001 Liaoning, People's Republic of China.
Xiaoqian ZhangDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang 110001 Liaoning, People's Republic of China.
Ying XuCancer Systems Biology Center, The China-Japan, Union Hospital, Jilin University, Changchun 130033 Jilin, People's Republic of China.
Chuansheng Zhao *Department of Neurology, The First Affiliated Hospital, China Medical University, Shenyang 110001 Liaoning, People's Republic of China.ORCID 0000-0002-4100-1259
Mei Zhao *Department of Cardiology, Sheng Jing Affiliated Hospital, China Medical University, Shenyang 110004 Liaoning, People's Republic of China.
First Hospital of China Medical University · CNUnion Hospital · CNSheng Jing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is associated with abnormal calcium signaling, a pathway regulated by the calcium-dependent protein phosphatase. This study aimed to investigate the molecular function of protein phosphatase 3 regulatory subunit B (PPP3R1) underlying AD, which may provide novel insights for the predictive diagnostics, targeted prevention, and personalization of medical services in AD by targeting PPP3R1. A total of 1860 differentially expressed genes (DEGs) from 13,049 background genes were overlapped in AD/control and PPP3R1-low/high cohorts. Based on these DEGs, six co-expression modules were constructed by weight gene correlation network analysis (WGCNA). The turquoise module had the strongest correlation with AD and low PPP3R1, in which DEGs participated in axon guidance, glutamatergic synapse, long-term potentiation (LTP), mitogen-activated protein kinase (MAPK), Ras, and hypoxia-inducible factor 1 (HIF-1) signaling pathways. Furthermore, the cross-talking pathways of PPP3R1, such as axon guidance, glutamatergic synapse, LTP, and MAPK signaling pathways, were identified in the global regulatory network. The area under the curve (AUC) analysis showed that low PPP3R1 could accurately predict the onset of AD. Therefore, our findings highlight the involvement of PPP3R1 in the pathogenesis of AD via axon guidance, glutamatergic synapse, LTP, and MAPK signaling pathways, and identify downregulation of PPP3R1 as a potential biomarker for AD treatment in the context of 3P medicine-predictive diagnostics, targeted prevention, and personalization of medical services. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13167-021-00261-2.

Indexed as

Alzheimer’s diseaseCo-expression networkDifferential expressionPathwayPPP3R1, protein phosphatase 3 regulatory subunit BPredictive preventive personalized medicine (PPPM)

Identifiers

PMID34956428
PMCPMC8648944
OpenAlexW3213927077

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.