Evidence map›Paper›PMID 41681058›Full record

ArticleAging cell2026

Adipose-Specific GHR Deletion Attenuates Brain Aging and Cognitive Decline in Aged Mice.

Yue Zhang, Rui Ma, Jia He, Liyuan Ran, Xuewei Yang, Yue Xi, Yingjie Wu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

7 authors.

Yue ZhangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Ophthalmology & Visual Science Key Laboratory, Beijing, China.
Rui MaInstitute for Genome Engineered Animal Models of Human Diseases, National Center of Genetically Engineered Animal Models for International Research, Liaoning Province Key Lab of Genetically Engineered Animal Models, Department of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Jia HeDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Liyuan RanKey Laboratory of Endocrine Glucose & Lipids Metabolism and Brain Aging, Ministry of Education, Shandong Provincial Hospital Affiliated to Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Xuewei YangDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Yue XiDepartment of Endocrinology and Metabolism, The Third Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, China.ORCID 0009-0004-2695-7502
Yingjie WuInstitute for Genome Engineered Animal Models of Human Diseases, National Center of Genetically Engineered Animal Models for International Research, Liaoning Province Key Lab of Genetically Engineered Animal Models, Department of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.ORCID 0000-0002-2694-1971

Funding

National Key Research and Development Program of China 2021YFA0805100National Key Research and Development Program of China 2021YFF0702100National Key Research and Development Program of China 2022YFE0132200National Natural Science Foundation of China 82101275National Natural Science Foundation of China 82370866
6 · The paper itself

Abstract

Brain aging is marked by neuronal loss, synaptic deterioration, neuroinflammation, and proteinopathies, all of which contribute to cognitive decline. Although systemic suppression of growth hormone (GH)/insulin-like growth factor-1 (IGF-1) signaling has been shown to extend lifespan and enhance cognitive function, the specific role of GH signaling in adipose tissue during brain aging remains unclear. In this study, we used aged (18-24 months) adipose-specific GH receptor knockout (Ad-GHRKO) mice and their littermate controls to investigate this relationship. We found that deletion of GHR in adipose tissue significantly attenuated key features of brain aging. Aged Ad-GHRKO mice exhibited reduced neuronal loss in the cortex and hippocampus, diminished neuroinflammation, decreased cellular senescence, and lower levels of tau phosphorylation in the hippocampus compared to controls. Additionally, synaptic integrity, indicated by hippocampal PSD95 expression, and cortical neuronal excitability were preserved. Importantly, Ad-GHRKO mice showed improved cognitive performance across multiple domains, including recognition memory (novel object recognition, NOR), working memory (Y-maze), spatial learning/memory (Morris water maze), and associative fear memory (passive avoidance). These findings suggest adipose GH signaling as a previously unrecognized peripheral regulator of brain aging and cognition, implicating adipose GHR as a therapeutic target for mitigating age-related cognitive decline.

Indexed as

Adipose TissueAgingBrainCognitive DysfunctionGene DeletionReceptors, SomatotropinAnimalsMaleMiceMice, Inbred C57BLMice, KnockoutReceptors, Somatotropinadipose tissuebrain agingcognitive declineGH/IGF‐1 axisgrowth hormone receptor

Identifiers

PMID41681058
PMCPMC12900898

What OpenQuestion holds

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Registered trials

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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.