Evidence map›Paper›PMID 40158900›Full record

ArticleThe journal of prevention of Alzheimer's disease2025

Fingolimod ameliorates amyloid deposition and neurodegeneration in APP/PS1 mouse model of Alzheimer's disease.

Meng-Ting Wang, Zi-Cheng Hu, Yang Xiang, Xiao-Qin Zeng, Zhang-Cheng Fei, Jia Chen, Xin-Peng Li, Yu-Peng Zhu, Jun Wang, Yan-Jiang Wang and 2 more

Abstract read
In one paragraph

Article in The journal of prevention of Alzheimer's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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

12 authors.

Meng-Ting WangDepartment of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, PR China.
Zi-Cheng HuDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, PR China.
Yang XiangInstitute of Neurology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, PR China.
Xiao-Qin ZengDepartment of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, PR China.
Zhang-Cheng FeiDepartment of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, PR China.
Jia ChenDepartment of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, PR China.
Xin-Peng LiDepartment of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, PR China.
Yu-Peng ZhuDepartment of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, PR China.
Jun WangDepartment of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, PR China.
Yan-Jiang WangDepartment of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, PR China; Key Laboratory of Aging and Brain Disease, Chongqing, PR China.
Zhi-Qiang XuDepartment of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, PR China. Electronic address: xzq881@163.com.
Yu-Hui LiuDepartment of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, PR China; Key Laboratory of Aging and Brain Disease, Chongqing, PR China. Electronic address: yuhuiliu@tmmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe immune system plays a critical role in regulating amyloid-beta (Aβ) metabolism in Alzheimer's Disease (AD). Both T and B lymphocytes are involved in the pathogenesis of AD. The sphingosine-1-phosphate (S1P) receptor modulator fingolimod used in the treatment of multiple sclerosis, can promote lymphocyte homing, potentially reducing the infiltration of peripheral lymphocytes into the brain.

methodsIn this study, 8-month-old APP/PS1 mice were orally administered fingolimod at a dose of 1 mg/kg/day or saline as a control for 2 months. After treatment, the mice were subjected to behavioral tests, pathological examinations, and biochemical analyses to evaluate behavioral deficits and AD-type pathologies.

resultsFingolimod inhibits the infiltration of peripheral lymphocytes into the brain and reduces neuroinflammation. Fingolimod enhances cognitive function and alleviates brain Aβ deposition. Additionally, fingolimod treatment mitigates other AD-related pathologies, including Tau hyperphosphorylation, neuroinflammation, and neurodegeneration. Proteomic analysis further confirms the therapeutic effects of fingolimod in AD, reflected by the downregulation of proteins involved in multiple AD-associated pathways. DISCUSSION: This study illustrates that fingolimod effectively ameliorates multiple pathological features of AD, highlighting its potential as a promising therapeutic candidate for the disease.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesFingolimod HydrochlorideSphingosine 1 Phosphate Receptor ModulatorsAmyloid beta-Protein PrecursorAnimalsBrainDisease Models, AnimalMiceMice, TransgenicPresenilin-1Amyloid beta-PeptidesAmyloid beta-Protein PrecursorFingolimod HydrochloridePresenilin-1Sphingosine 1 Phosphate Receptor ModulatorsAlzheimerAmyloid-betaFingolimodLymphocyteNeurodegeneration

Identifiers

PMID40158900
PMCPMC12321628

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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.