Evidence map›Paper›PMID 33186918›Full record

ArticleAging2020

Molecular identification of protein kinase C beta in Alzheimer's disease.

Zhike Zhou, Fenqin Chen, Shanshan Zhong, Yi Zhou, Rongwei Zhang, Kexin Kang, Xiaoqian Zhang, Ying Xu, Mei Zhao, Chuansheng Zhao

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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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

10 authors at 3 institutions in 2 countries.

Zhike ZhouDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China.
Fenqin ChenDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China.
Shanshan ZhongDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China.
Yi ZhouComputational Systems Biology Lab, Department of Biochemistry and Molecular Biology and Institute of Bioinformatics, The University of Georgia, Athens, GA 30602, USA.
Rongwei ZhangDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China.
Kexin KangDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China.
Xiaoqian ZhangDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China.
Ying XuComputational Systems Biology Lab, Department of Biochemistry and Molecular Biology and Institute of Bioinformatics, The University of Georgia, Athens, GA 30602, USA.
Mei ZhaoDepartment of Cardiology, The Shengjing Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China.
Chuansheng ZhaoDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning, PR China.
First Hospital of China Medical University · CNChina Medical University · CNUniversity of Georgia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of this study was to investigate the potential roles of protein kinase C beta (PRKCB) in the pathogenesis of Alzheimer's disease (AD). We identified 2,254 differentially expressed genes from 19,245 background genes in AD versus control as well as PRKCB-low versus high group. Five co-expression modules were constructed by weight gene correlation network analysis. Among them, the 1,222 genes of the turquoise module had the strongest relation to AD and those with low PRKCB expression, which were enriched in apoptosis, axon guidance, gap junction, Fc gamma receptor (FcγR)-mediated phagocytosis, mitogen-activated protein kinase (MAPK) and vascular endothelial growth factor (VEGF) signaling pathways. The intersection pathways of PRKCB in AD were determined, including gap junction, FcγR-mediated phagocytosis, MAPK and VEGF signaling pathways. Based on the performance evaluation of the area under the curve of 75.3%, PRKCB could accurately predict the onset of AD. Therefore, low expressions of PRKCB was a potential causative factor of AD, which might be involved in gap junction, FcγR-mediated phagocytosis, MAPK and VEGF signaling pathways.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseFemaleGene Expression ProfilingHumansMaleProtein Kinase C betaSignal TransductionTranscriptomeProtein Kinase C betaAlzheimer's diseasegene expressionnetworkPRKCB

Identifiers

PMID33186918
PMCPMC7695410
OpenAlexW3101220685

What OpenQuestion holds

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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 OpenQuestion graph.