Evidence map›Paper›PMID 35732922›Full record

ArticleCell death and differentiation2022

CEND1 deficiency induces mitochondrial dysfunction and cognitive impairment in Alzheimer's disease.

Wenting Xie, Dong Guo, Jieyin Li, Lei Yue, Qi Kang, Guimiao Chen, Tingwen Zhou, Han Wang, Kai Zhuang, Lige Leng and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 5% of its field
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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

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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

14 authors at 3 institutions in 1 country.

Wenting Xie *Institute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian, 361005, China.
Dong Guo *Institute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian, 361005, China.ORCID 0000-0001-7057-2838
Jieyin Li *Institute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian, 361005, China.
Lei YueFujian Key Laboratory of Molecular Neurology, Institute of Neuroscience, Fujian Medical University, Fuzhou, Fujian, 350004, China.
Qi KangInstitute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian, 361005, China.
Guimiao ChenInstitute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian, 361005, China.
Tingwen ZhouInstitute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian, 361005, China.
Han WangInstitute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian, 361005, China.
Kai ZhuangInstitute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian, 361005, China.
Lige LengInstitute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian, 361005, China.
Huifang LiInstitute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian, 361005, China.
Zhenyi ChenDepartment of Anesthesiology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, 361005, China.
Weiwei GaoFujian Key Laboratory of Molecular Neurology, Institute of Neuroscience, Fujian Medical University, Fuzhou, Fujian, 350004, China. gaoww@fjmu.edu.cn.ORCID 0000-0002-3120-4466
Jie ZhangInstitute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian, 361005, China. jiezhang@xmu.edu.cn.ORCID 0000-0003-1040-5848
Xiamen University · CNFujian Medical University · CNFirst Affiliated Hospital of Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common form of neurodegenerative disease featured with memory loss and cognitive function impairments. Chronic mitochondrial stress is a vital pathogenic factor for AD and finally leads to massive neuronal death. However, the underlying mechanism is unclear. By proteomic analysis, we identified a new mitochondrial protein, cell-cycle exit and neuronal differentiation 1 (CEND1), which was decreased significantly in the brain of 5xFAD mice. CEND1 is a neuronal specific protein and locates in the presynaptic mitochondria. Depletion of CEND1 leads to increased mitochondrial fission mediated by upregulation of dynamin related protein 1 (Drp1), resulting in abnormal mitochondrial functions. CEND1 deficiency leads to cognitive impairments in mice. Overexpression of CEND1 in the hippocampus of 5xFAD mice rescued cognitive deficits. Moreover, we identified that CDK5/p25 interacted with and phosphorylated CEND1 which promoted its degradation. Our study provides new mechanistic insights in mitochondrial function regulations by CEND1 in Alzheimer's disease.

Indexed as

Alzheimer DiseaseCognitive DysfunctionNeurodegenerative DiseasesAmyloid beta-PeptidesAnimalsDisease Models, AnimalMembrane ProteinsMiceMice, TransgenicMitochondriaNerve Tissue ProteinsProteomicsAmyloid beta-PeptidesCend1 protein, mouseMembrane ProteinsNerve Tissue Proteins

Identifiers

PMID35732922
PMCPMC9751129
OpenAlexW4283260243

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.