Evidence map›Paper›PMID 40586131›Full record

ArticleCNS neuroscience & therapeutics2025

Downregulation of USP9X in the DG Region of the Hippocampus Leads to AD-Like Cognitive Dysfunction in Mice.

Xiaochuan Qi, Mengjiao Ying, Ao Wang, Kelin Shi, Guangshang Zhong, Yichao Lu, Changqing Liu, Yu Guo

Abstract read
PubMed Full text at PMC Publisher
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Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Molecular medicine reports · 2026
    Article
  2. Article
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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

8 authors.

Xiaochuan QiAnhui Engineering Research Centre for Neural Regeneration Technology and Medical New Materials, Bengbu Medical University, Bengbu, China.ORCID 0009-0009-1478-8592
Mengjiao YingAnhui Engineering Research Centre for Neural Regeneration Technology and Medical New Materials, Bengbu Medical University, Bengbu, China.ORCID 0009-0007-0914-9193
Ao WangAnhui Engineering Research Centre for Neural Regeneration Technology and Medical New Materials, Bengbu Medical University, Bengbu, China.ORCID 0009-0007-4585-2097
Kelin ShiAnhui Engineering Research Centre for Neural Regeneration Technology and Medical New Materials, Bengbu Medical University, Bengbu, China.
Guangshang ZhongAffiliated Hospital of Shandong University of Traditional Chinese Medicine, Pathology, Jinan, China.
Yichao LuSchool of Clinical Medicine, Bengbu Medical University, Bengbu, China.
Changqing LiuAnhui Engineering Research Centre for Neural Regeneration Technology and Medical New Materials, Bengbu Medical University, Bengbu, China.
Yu GuoAnhui Engineering Research Centre for Neural Regeneration Technology and Medical New Materials, Bengbu Medical University, Bengbu, China.

Funding

Anhui Provincial Key Research and Development Project 2022e07020030Anhui Provincial Key Research and Development Project 2022e07020032Anhui Provincial Natural Science Foundation 2308085MH256Longhu Talent Project of Bengbu Medical University LH250102002National Natural Science Foundation of China 82371382the Postgraduate Innovative Training Program of Bengbu Medical College Byycxz24033the Undergraduate Innovative Training Program of China 202410367012the Undergraduate Innovative Training Program of China 202410367024
6 · The paper itself

Abstract

objectiveThis study investigates the link between ubiquitin-specific peptidase 9 X-linked (USP9X) and Alzheimer's disease (AD) pathogenesis, aiming to identify potential targets for AD diagnosis, treatment, and drug development.

methodsWe constructed a USP9X-inhibited expression mouse model and assessed cognitive and memory functions. We also measured Tau phosphorylation and APP levels in the hippocampal dentate gyrus (DG) and analyzed neuronal functions, dendritic spine features, late apoptosis, and autophagy.

resultsMice with USP9Xinhibition exhibited impaired cognitive and memory functions. An increase in the APP levels and Tau hyperphosphorylation in the DG resembled AD-like pathology. Neurons exhibited abnormal functions, altered dendritic spine morphology, increase in neuronal apoptosis, and dysfunctions, similar to neuron loss observed in AD.

conclusionInvestigating the role of USP9X in AD could provide valuable insights for developing novel diagnostic and therapeutic strategies for AD.

Indexed as

Alzheimer DiseaseCognitive DysfunctionDentate GyrusUbiquitin ThiolesteraseAnimalsDisease Models, AnimalDown-RegulationHippocampusMaleMiceMice, Inbred C57BLMice, TransgenicUbiquitin ThiolesteraseUsp9x protein, mouseAlzheimer's diseasecognitive impairmentfunction researchneuronal dysfunctionUSP9X

Identifiers

PMID40586131
PMCPMC12207322

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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.