Evidence map›Paper›PMID 42596624›Full record

ArticleCNS neuroscience & therapeutics2026

A Novel Nogo-A Receptor Antagonist Peptide Impedes Alzheimer's Disease Pathology by Nogo-A/NgR/ROCK Signaling Pathway.

Zheng Zhang, Huimin Tan, Fang Shi, Jiajia Dai, Weilong Ding, Junliang Li, Yuke Wang, Rui Yang, Xinke Xu, Cheng Chen and 5 more

Abstract read
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In one paragraph

Article in CNS neuroscience & therapeutics, 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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1 · What the graph read from it

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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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3 · Its place in the literature

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4 · The record

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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

15 authors.

Zheng ZhangDepartment of Pharmacy, The First Affiliated Hospital of Jinan University, Jinan University, Guangzhou, Guangdong Province, China.
Huimin TanDepartment of Neurology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong Province, China.
Fang ShiFormula-Pattern Research Center, School of Traditional Chinese Medicine, Jinan University, Guangzhou, China.
Jiajia DaiDepartment of Pharmacology, School of Medicine, Jinan University, Guangzhou, Guangdong Province, China.
Weilong DingDepartment of Neurosurgery, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Junliang LiDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong Province, China.
Yuke WangSchool of Medicine, Jinan University, Guangzhou, Guangdong Province, China.
Rui YangDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong Province, China.
Xinke XuDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong Province, China.
Cheng ChenDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong Province, China.
Fei XiaoDepartment of Pharmacology, School of Medicine, Jinan University, Guangzhou, Guangdong Province, China.
Li-An HuangDepartment of Neurology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong Province, China.ORCID https://orcid.org/0000-0002-4533-0535
Xiaoyan LiuDepartment of Neurology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong Province, China.
Rui LiaoThe First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, Guangdong Province, China.
Li YanFormula-Pattern Research Center, School of Traditional Chinese Medicine, Jinan University, Guangzhou, China.ORCID https://orcid.org/0000-0001-7232-8353

Funding

2024 Joint between City, University (College) and Enterprise 2024A03J0902Basic and Applied Basic Research Foundation of Guangdong Province 2026A1515011575Fundamental Research Funds for the Central Universities 21626406Guangdong Provincial Medical Science and Technology Research Fund 20211128182437730Horizontal Research from the Guangdong Provincial Health Economics Association 2025-WJHX-31National Natural Science Foundation of China 82102690
6 · The paper itself

Abstract

aimsTo evaluate the therapeutic effects of NAP2, a novel NgR1 antagonist peptide, on Alzheimer's disease (AD) pathology and to determine whether inhibition of the Nogo-A/NgR1/ROCK signaling axis can ameliorate neurodegenerative alterations in APP/PS1 mice.

methodsAPP/PS1 transgenic mice received a three-month NAP2 intervention. Cognitive performance was assessed using standard learning and memory tests. Amyloid-β plaque burden, dendritic spine density, tau phosphorylation, and Aβ42 levels were examined by histological and biochemical analyses. Mitochondrial function and downstream ROCK signaling activity were also evaluated.

resultsNAP2 treatment significantly improved cognitive performance in APP/PS1 mice. NAP2 reduced amyloid-β plaque deposition, decreased Aβ42 expression, and increased hippocampal dendritic spine density. Tau hyperphosphorylation was notably attenuated. In addition, NAP2 alleviated Aβ42-induced mitochondrial dysfunction. Mechanistic studies revealed that NAP2 interfered with ROCK signaling downstream of Nogo-A.

conclusionNAP2 ameliorates multiple AD-related pathological features, an effect accompanied by the inhibition of the Nogo-A/NgR1/ROCK pathway. These findings highlight the therapeutic potential of NAP2 to enhance resilience against Alzheimer's disease pathology.

Indexed as

Alzheimer DiseaseNogo ProteinsNogo Receptor 1Peptidesrho-Associated KinasesSignal TransductionAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalHumansMaleMiceMice, TransgenicPeptide FragmentsPresenilin-1Amyloid beta-Peptidesamyloid beta-protein (1-42)Amyloid beta-Protein PrecursorNogo ProteinsNogo Receptor 1Peptide FragmentsPeptidesPresenilin-1rho-Associated KinasesRtn4 protein, mouseRtn4r protein, mousetau ProteinsAlzheimer's diseaseAβ peptidesNogo‐A receptor antagonist peptide 2(NAP2)

Identifiers

PMID42596624
PMCPMC13473841

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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.