Evidence map›Paper›PMID 41526711›Full record

ArticleCommunications medicine2026

Metabolism fluctuation coupling can track the progression of dementia and describe MST1 gene-related pathology.

Jinhua Sheng, Ze Yang, Yang Wang, Qiao Zhang, Yu Xin, Yan Song, Luyun Wang

Abstract read
In one paragraph

Article in Communications medicine, 2026. 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

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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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Jinhua ShengSchool of Computer Science and Technology, Hangzhou Dianzi University, Hangzhou, Zhejiang, China. j.sheng@ieee.org.ORCID http://orcid.org/0000-0002-7662-9126
Ze YangSchool of Computer Science and Technology, Hangzhou Dianzi University, Hangzhou, Zhejiang, China.
Yang WangDepartment of Radiology, Medical College of Wisconsin, Wauwatosa, WI, USA.
Qiao ZhangBeijing Hospital, Beijing, China.
Yu XinSchool of Computer Science and Technology, Hangzhou Dianzi University, Hangzhou, Zhejiang, China.
Yan SongBeijing Hospital, Beijing, China.
Luyun WangSchool of Computer Science and Technology, Hangzhou Dianzi University, Hangzhou, Zhejiang, China.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 62271177Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LZ24F01007
6 · The paper itself

Abstract

backgroundCognitive resilience refers to an individual's capacity to cope with brain aging and pathology and to delay cognitive decline, whereas existing techniques such as functional magnetic resonance imaging capture only macroscopic features without linking them to neurophysiological mechanisms. Recent studies have shown that overexpression of the MST1 gene exacerbates Alzheimer's disease phenotypes by affecting neuronal activity and metabolism; however, its association with cognitive trajectories and imaging biomarkers remains to be further investigated.

methodsMultimodal imaging data using information from 116 individuals with mild cognitive impairment was obtained from the ADNI database and participants from the HABS database. The correlation coefficient between glucose metabolism and neuronal low-frequency fluctuations was calculated, and residuals were derived from regression models of correlation coefficient with amyloid protein. Unsupervised clustering was then applied, and mediation analysis was conducted to investigate the mediating role of limbic orbital frontal cortex residuals in the association between MST1 gene expression and cognitive trajectories.

resultsClustering identifies five groups with distinct cognitive trajectories: the high and low cognitive resilience groups exhibit slower dementia progression with lower MST1 expression, whereas the high and low cognitive vulnerability groups show faster dementia progression with higher MST1 expression. No significant differences are observed in glucose metabolism or amyloid protein levels across groups, while the limbic orbital frontal cortex residuals partially mediate the effect of MST1 gene expression on cognitive trajectories.

conclusionsResidual biomarkers can track dementia progression and characterize MST1-related pathology, providing imaging markers for assessing cognitive resilience and monitoring disease at the molecular level.

Identifiers

PMID41526711
PMCPMC12796309

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