Evidence map›Paper›PMID 41689616›Full record

ArticleMolecular neurobiology2026

ARC-18 Alleviates Alzheimer-like Pathology and Cognitive Deficits via AdipoR1-Mediated Activation of Autophagy and Modulation of APP Processing.

Shangming Li, Bocheng Xiong, Nan Xu, Lulin Nie, Kaiwu He, Guiliang Zhang, Chongyang Chen, Zaijun Zhang, Maggie Pui Man Hoi, Xifei Yang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 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

10 authors.

Shangming LiKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Bocheng XiongKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Nan XuState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Avenida da Universiade, Taipa, Macau, N22-7012, China.
Lulin NieKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Kaiwu HeKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Guiliang ZhangState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Avenida da Universiade, Taipa, Macau, N22-7012, China.
Chongyang ChenKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Zaijun ZhangGuangdong Province Key Laboratory of Pharmacodynamic, Constituents of Traditional Chinese Medicine & New Drug Research, Institute of New Drug Research, College of Pharmacy, Jinan University, Guangdong, China.
Maggie Pui Man HoiState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Avenida da Universiade, Taipa, Macau, N22-7012, China. maghoi@um.edu.mo.
Xifei YangKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China. xifeiyang@gmail.com.ORCID http://orcid.org/0000-0002-9000-7016

Funding

Sanming Project of Medicine in Shenzhen SZSM202211010the Science and Technology Development Fund of the Macao SAR FDCT/0023/2020/AFJthe University of Macau Research Funding MYRG2022-00248-ICMS
6 · The paper itself

Abstract

Alzheimer's disease (AD), the most prevalent form of dementia, is characterized as a slowly progressing neurodegenerative disease marked by senile plaques and neurofibrillary tangles due to the buildup of amyloid-beta peptide (Aβ) and phosphorylated tau in the brain. It is reported that arctigenin (ATG) reduces the level of the enzyme 1 that cleaves β-site amyloid precursor protein and increases Aβ clearance by enhancing autophagy. Compound ARC-18 is a derivative of ATG. The main objective of this study is to investigate whether ARC-18 could improve cognitive function and disease progression by promoting autophagy in Alzheimer-like animal models. Three-month-old 5 × FAD mice were orally treated with the drug for three consecutive months. Water maze and novel object recognition were used to assess cognitive abilities of 5 × FAD mice. In the hippocampus of the mice' brain, APP processing-related proteins (sAPP

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAutophagyCognition DisordersFuransLignansReceptors, AdiponectinAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAnimalsHippocampusMaleMaze LearningMiceMice, TransgenicAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesFuransLignansReceptors, Adiponectin5 × FAD miceAdiponectin receptor 1Alzheimer’s diseaseARC-18Autophagy

Identifiers

PMID41689616

What OpenQuestion holds

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Registered trials

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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.