Evidence map›Paper›PMID 41419666›Full record

ArticleNature aging2026

CDK3 induces neuronal death and brain atrophy in Alzheimer's disease.

Kai Zhuang, Liu Zi, Xiao Su, Chen Hu, Xinrui Li, Shuzhong Wang, Yujun Xia, Bo Wu, Yuemin Su, Shaokun Chen and 14 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature aging, 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

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

1 citing paper in PubMed.

  1. 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

24 authors.

Kai Zhuang *Institute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Liu Zi *Institute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Xiao SuInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Chen HuInstitute of Health and Medical Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, China.
Xinrui LiInstitute for Stem Cell and Neural Regeneration, School of Pharmacy, Nanjing Medical University, Nanjing, China.
Shuzhong WangInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Yujun XiaInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Bo WuInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Yuemin SuInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Shaokun ChenInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Haojie LiTenth People's Hospital of Tongji University, Shanghai, China.
Siqi WangInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.ORCID http://orcid.org/0000-0001-6467-4416
Mengdan WangInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Jieyin LiInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Wenting XieInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Yanbing ChenInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Lige LengInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.ORCID http://orcid.org/0000-0002-4288-4743
Huifang LiInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Li ZhongInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.ORCID http://orcid.org/0000-0003-3815-6484
Jiechao ZhouInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Yan LiuInstitute for Stem Cell and Neural Regeneration, School of Pharmacy, Nanjing Medical University, Nanjing, China.ORCID http://orcid.org/0000-0003-2918-5398
Qingsong LiuInstitute of Health and Medical Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, China.ORCID http://orcid.org/0000-0002-7829-2547
Karl HerrupDepartment of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.ORCID http://orcid.org/0000-0001-7786-5844
Jie ZhangInstitute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China. jiezhang@xmu.edu.cn.ORCID http://orcid.org/0000-0003-1040-5848

Funding

China Postdoctoral Science Foundation 2020M682094National Natural Science Foundation of China (National Science Foundation of China) 82101242 and 32371505National Natural Science Foundation of China (National Science Foundation of China) 82530048, U23A20430, 81925010, 91849205 and 92149303Pennsylvania Department of State (DOS) 4100087331U.S. Department of Health & Human Services | National Institutes of Health (NIH) R01NS120922 and R01AG069912
6 · The paper itself

Abstract

Progressive neuronal loss and brain atrophy are principal determinants of cognitive decline in Alzheimer's disease (AD), yet most mouse models fail to recapitulate these features. Here we identify cyclin-dependent kinase 3 (CDK3) as a key driver of neurodegeneration in AD. CDK3 is elevated in human AD brains and correlates with disease severity. As laboratory mice carry a nonfunctional Cdk3 mutation, we generated two models with restored CDK3 activity and then crossed to AD backgrounds. Both models exhibited substantial neuronal loss, hippocampal atrophy, and cognitive deficits. Single-nucleus RNA sequencing revealed neurons simultaneously activating cell cycle and cell death pathways, indicating cell cycle reentry-induced death. Proteomics implicated synaptic proteins as CDK3 substrates. Finally, we developed BMX330, an inhibitor of CDK3, which mitigated neuronal death and rescued cognitive decline in CDK3-restored AD mice. These findings position CDK3 as a therapeutic target and provide pathologically relevant AD models.

Indexed as

Alzheimer DiseaseBrainNeuronsAnimalsAtrophyCell DeathCognitive DysfunctionDisease Models, AnimalFemaleHippocampusHumansMaleMiceMice, Transgenic

Identifiers

PMID41419666

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.