Evidence map›Paper›PMID 35571248›Full record

ArticleOxidative medicine and cellular longevity2022

Down-Regulation of Insulin Like Growth Factor 1 Involved in Alzheimer's Disease via MAPK, Ras, and FoxO Signaling Pathways.

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

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. 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
1.6field-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

12 citing papers in PubMed, 19 citations in OpenAlex.

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  11. Effects of fasting onHeliyon · 2023
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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 4 institutions in 2 countries.

Kexin KangDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang, 110001 Liaoning, China.ORCID https://orcid.org/0000-0002-7124-3240
Jun BaiCancer Systems Biology Center, The China-Japan Union Hospital, Jilin University, Changchun, 130033 Jilin, China.
Shanshan ZhongDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang, 110001 Liaoning, China.
Rongwei ZhangDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang, 110001 Liaoning, China.
Xiaoqian ZhangDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang, 110001 Liaoning, China.
Ying XuCancer Systems Biology Center, The China-Japan Union Hospital, Jilin University, Changchun, 130033 Jilin, China.
Mei ZhaoDepartment of Cardiology, The Shengjing Affiliated Hospital, China Medical University, Shenyang, 110004 Liaoning, China.ORCID https://orcid.org/0000-0003-4204-9235
Chuansheng ZhaoDepartment of Neurology, The First Affiliated Hospital, China Medical University, Shenyang, 110001 Liaoning, China.ORCID https://orcid.org/0000-0002-4100-1259
Zhike ZhouDepartment of Geriatrics, The First Affiliated Hospital, China Medical University, Shenyang, 110001 Liaoning, China.ORCID https://orcid.org/0000-0002-3571-8130
First Hospital of China Medical University · CNChina Medical University · CNJilin University · CNUniversity of Georgia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inability to halt or even delay the course of Alzheimer's disease (AD) forces the development of new molecular signatures and therapeutic strategies. Insulin like growth factor 1 (IGF1) is a promising target for AD treatment, yet exact mechanisms of AD ascribed to IGF1 remain elusive. Herein, gene expression profiles of 195 samples were analyzed and 19,245 background genes were generated, among which 4,424 differentially expressed genes (DEGs) were overlapped between AD/control and IGF1-low/high groups. Based on such DEGs, seven co-expression modules were established by weight gene correlation network analysis (WGCNA). The turquoise module had the strongest correlation with AD and IGF1-low expression, the DEGs of which were enriched in GABAergic synapse, long-term potentiation, mitogen-activated protein kinase (MAPK), Ras, and forkhead box O (FoxO) signaling pathways. Furthermore, cross-talking pathways of IGF1, including MAPK, Ras, and FoxO signaling pathways were identified in the protein-protein interaction network. According to the area under the curve (AUC) analysis, down-regulation of IGF1 exhibited good diagnostic performance in AD prediction. Collectively, our findings highlight the involvement of low IGF1 in AD pathogenesis via MAPK, Ras, and FoxO signaling pathways, which might advance strategies for the prevention and therapy of AD based on IGF1 target.

Indexed as

Alzheimer DiseaseDown-RegulationGene Expression ProfilingHumansInsulin-Like Growth Factor IMitogen-Activated Protein KinasesSignal TransductionInsulin-Like Growth Factor IMitogen-Activated Protein Kinases

Identifiers

PMID35571248
PMCPMC9096571
OpenAlexW4229057485

What OpenQuestion holds

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LicenceCC BY
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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.