Evidence map›Paper›PMID 40296620›Full record

ArticleCurrent Alzheimer research2025

NRN1 may Modulate Tau Phosphorylation and Neuronal Apoptosis in AD

Wenshuo Cheng, Jia Zhang, Hui Zhu, Zhenyu Wang, Min Li, Junyi Wang, Hongdan Fu, Yutai Zhang, Yuhang Gao, Changyu Chen and 3 more

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Article in Current Alzheimer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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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

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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

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

13 authors.

Wenshuo ChengThe Key Laboratory of Xinjiang Endemic and Ethnic Diseases and Department of Biochemistry, Shihezi University School of Medicine, Shihezi, 832003, China.
Jia ZhangThe Key Laboratory of Xinjiang Endemic and Ethnic Diseases and Department of Biochemistry, Shihezi University School of Medicine, Shihezi, 832003, China.
Hui ZhuDepartment of Otorhinolaryngology, The First Affiliated Hospital, Shihezi University, Shihezi, 832008, China.
Zhenyu WangThe Key Laboratory of Xinjiang Endemic and Ethnic Diseases and Department of Biochemistry, Shihezi University School of Medicine, Shihezi, 832003, China.
Min LiShihezi University Nursing School, Shihezi, 832003, China.
Junyi WangThe Key Laboratory of Xinjiang Endemic and Ethnic Diseases and Department of Biochemistry, Shihezi University School of Medicine, Shihezi, 832003, China.
Hongdan FuThe Key Laboratory of Xinjiang Endemic and Ethnic Diseases and Department of Biochemistry, Shihezi University School of Medicine, Shihezi, 832003, China.
Yutai ZhangThe Key Laboratory of Xinjiang Endemic and Ethnic Diseases and Department of Biochemistry, Shihezi University School of Medicine, Shihezi, 832003, China.
Yuhang GaoThe Key Laboratory of Xinjiang Endemic and Ethnic Diseases and Department of Biochemistry, Shihezi University School of Medicine, Shihezi, 832003, China.
Changyu ChenThe Key Laboratory of Xinjiang Endemic and Ethnic Diseases and Department of Biochemistry, Shihezi University School of Medicine, Shihezi, 832003, China.
Cunhu YuanThe Key Laboratory of Xinjiang Endemic and Ethnic Diseases and Department of Biochemistry, Shihezi University School of Medicine, Shihezi, 832003, China.
Jingling ZhuThe Key Laboratory of Xinjiang Endemic and Ethnic Diseases and Department of Biochemistry, Shihezi University School of Medicine, Shihezi, 832003, China.ORCID 0000-0003-3667-6347
Jiawei SunThe Key Laboratory of Xinjiang Endemic and Ethnic Diseases and Department of Biochemistry, Shihezi University School of Medicine, Shihezi, 832003, China.ORCID 0000-0002-9527-0219

Funding

Natural Science Foundation of China 81771173Scientific Research Fund of Shihezi University CXPY202310, ZZZC202138Training Program for Undergraduates of Shihezi University SRP2024440
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by hyperphosphorylation of tau protein to form neurofibrillary tangles (NFTs) and amyloid β (Aβ) deposition to form senile plaques, and its specific regulatory mechanism remains incompletely understood. Neurotrophic factors (NTFs) play important roles in neuronal growth, differentiation, and survival, and are considered to have potential therapeutic effects in AD.

objectiveThis study aimed to investigate the effects of NTFs on tau protein phosphorylation in AD and its underlying mechanisms.

methodsA correlation analysis was conducted between neurotrophic factors and tau protein phosphorylation genes using bioinformatics analysis. The relationship between the candidate neurotrophic factor NRN1 and tau protein phosphorylation was validated

resultsBioinformatics analysis revealed a significant negative correlation between NRN1 and MAPT, a gene linked to tau protein phosphorylation. Western blot analysis indicated a decrease in NRN1 expression and an increase in p-tau levels in the hippocampus of AD mice. NRN1 significantly reduced the expression of p-tau in AD cell models and enhanced the expression of MAP2, a protein related to neural processes. Further, apoptosis analysis demonstrated that NRN1 significantly decreased the level of cleaved caspase-3 and elevated the Bcl-2/Bax ratio. Bioinformatics analysis and PPI network construction suggested PIGU and CASP3 to play pivotal roles in NRN1 regulation of tau protein phosphorylation.

conclusionNRN1 may mitigate tau protein phosphorylation and neuronal apoptosis by modulating the PIGU-CASP3 pathway in AD. This finding offers novel insights into NRN1 as a potential target for the treatment of AD.

Indexed as

Alzheimer DiseaseApoptosisCaspase 3Neuronstau ProteinsAnimalsDisease Models, AnimalHumansMaleMicePhosphorylationCaspase 3tau ProteinsAlzheimer's diseasebioinformaticsCASP3.neurotrophic factorNRN1tau phosphorylation

Identifiers

PMID40296620

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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.