Evidence map›Paper›PMID 41631736›Full record

ArticleHistology and histopathology2026

Tyrosine protein kinase ABL1 regulates the mTOR/ULK1 pathway to alleviate postoperative cognitive dysfunction in aged mice.

Chanjuan Chen, Jingwen Hao, Yuan Liu, Qi Wan

Abstract read
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In one paragraph

Article in Histology and histopathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Chanjuan ChenDepartment of Neurology, The First Hospital of Changsha, Changsha, Hunan, China.
Jingwen HaoDepartment of Neurology, The First Hospital of Changsha, Changsha, Hunan, China.
Yuan LiuDepartment of Neurology, The First Hospital of Changsha, Changsha, Hunan, China.
Qi WanDepartment of Neurology, The First Hospital of Changsha, Changsha, Hunan, China. wanqi0176@126.com.

Funding

Changsha Municipal Health Commission B202312Changsha Municipal Health Commission KJ-B2023045
6 · The paper itself

Abstract

backgroundPostoperative cognitive dysfunction (POCD) is a common and serious complication in older adult patients. While the tyrosine kinase ABL1 has been implicated in neurodegenerative diseases, its specific role in POCD remains unexplored. This study aims to investigate whether ABL1 influences POCD in aged mice by regulating microglial autophagy and neuroinflammation via the mTOR/ULK1 pathway.

methodsAn aged mouse model of POCD was established, and ABL1 silencing and 3-Methyladenine (3-MA) were used to intervene in mice. The Novel Object Recognition Test (NORT) assessment and water maze experiment were conducted. qRT-PCR quantified the mRNA levels of inflammatory cytokines, hippocampal damage was assessed by immunofluorescence, and western blot analyzed the protein expression of autophagy-related genes and the mTOR/ULK1 pathway. Co-Immunoprecipitation (CO-IP) was used to detect the binding of ABL1 to mTOR.

results

conclusions

Indexed as

Autophagy-Related Protein-1 HomologIntracellular Signaling Peptides and ProteinsPostoperative Cognitive ComplicationsProto-Oncogene Proteins c-ablTOR Serine-Threonine KinasesAgingAnimalsAutophagyDisease Models, AnimalHippocampusMaleMiceMice, Inbred C57BLMicrogliaSignal TransductionAutophagy-Related Protein-1 HomologIntracellular Signaling Peptides and ProteinsmTOR protein, mouseProto-Oncogene Proteins c-ablTOR Serine-Threonine KinasesUlk1 protein, mouse

Identifiers

PMID41631736

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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.