Evidence map›Paper›PMID 42401549›Full record

ArticleTranslational psychiatry2026

Maraviroc attenuates inflammation-exacerbated cognitive and amyloid pathology in an early-stage Alzheimer's disease mouse model.

Chang Liu, Ting Zhang, Er-Deng E, Tian-Yang Xu, Fei-Ran Yang, Jia-Wen Li, Qing Shang, Zhong-Yu Zhang, Hao-Wei Shen, Xiao-Qin Zhang

Abstract read
In one paragraph

Article in Translational psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Chang LiuDepartment of Pharmacology, Health Science Center, Zhejiang Key Laboratory of Drug Addiction and Brain Health, Ningbo University, Ningbo, Zhejiang, China.
Ting ZhangDepartment of Pharmacology, Health Science Center, Zhejiang Key Laboratory of Drug Addiction and Brain Health, Ningbo University, Ningbo, Zhejiang, China.
Er-Deng EDepartment of Pharmacology, Health Science Center, Zhejiang Key Laboratory of Drug Addiction and Brain Health, Ningbo University, Ningbo, Zhejiang, China.
Tian-Yang XuDepartment of Pharmacology, Health Science Center, Zhejiang Key Laboratory of Drug Addiction and Brain Health, Ningbo University, Ningbo, Zhejiang, China.
Fei-Ran YangDepartment of Pharmacology, Health Science Center, Zhejiang Key Laboratory of Drug Addiction and Brain Health, Ningbo University, Ningbo, Zhejiang, China.
Jia-Wen LiDepartment of Pharmacology, Health Science Center, Zhejiang Key Laboratory of Drug Addiction and Brain Health, Ningbo University, Ningbo, Zhejiang, China.
Qing ShangDepartment of Cerebrovascular Disease, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang, China.
Zhong-Yu ZhangKey Laboratory of Addiction Research, The Affiliated Kangning Hospital of Ningbo University, Ningbo, Zhejiang, China.
Hao-Wei ShenDepartment of Pharmacology, Health Science Center, Zhejiang Key Laboratory of Drug Addiction and Brain Health, Ningbo University, Ningbo, Zhejiang, China.
Xiao-Qin ZhangDepartment of Pharmacology, Health Science Center, Zhejiang Key Laboratory of Drug Addiction and Brain Health, Ningbo University, Ningbo, Zhejiang, China. zhangxiaoqin1@nbu.edu.cn.ORCID http://orcid.org/0000-0003-0254-7598

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32201322Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LY24H090001
6 · The paper itself

Abstract

Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by progressive cognitive decline, and increasing evidence indicates that systemic inflammation can accelerate disease progression. Maraviroc, a CCR5 antagonist approved for the treatment of human immunodeficiency virus (HIV) infection, has shown neuroprotective effects in several neurological contexts, but its role in AD-related pathology remains unclear. In this study, cognitive performance was assessed in 5 × FAD mice using the Y-maze, novel object recognition, novel location recognition, and social discrimination tests. Amyloid-related changes were evaluated by hippocampal APP/Aβ immunoblotting and plaque staining using 6E10 and Thioflavin S. Glial responses were examined by IBA1 and GFAP immunostaining, and inflammatory cytokines were quantified by ELISA. We found that 5 × FAD mice exhibited age-dependent cognitive impairments, with detectable deficits emerging at 3 months of age. Systemic administration of lipopolysaccharide (LPS) further exacerbated cognitive dysfunction, amyloid-related alterations, and neuroinflammatory responses in young 5 × FAD mice. Maraviroc treatment attenuated LPS-associated cognitive impairments, reduced amyloid-related measures, and dampened pro-inflammatory cytokine responses, with a trend toward reduced microglial cell density. Collectively, these findings demonstrate that systemic inflammation accelerates Alzheimer's-like pathology and cognitive decline, and suggest that pharmacological modulation of neuroinflammatory signaling by maraviroc may mitigate inflammation-driven disease exacerbation at early stages. Schematic diagram illustrating the effects of maraviroc on LPS-induced cognitive deficits in 3-month-old 5 × FAD mice. In this model, maraviroc is associated with modulation of glial inflammatory responses, reduced pro-inflammatory cytokine levels, and alleviation of amyloid pathology in the hippocampus, which together coincide with improved cognitive performance. Figure created with BioRender.com.

Indexed as

Alzheimer DiseaseCCR5 Receptor AntagonistsCognitive DysfunctionInflammationMaravirocAmyloid beta-PeptidesAnimalsCytokinesDisease Models, AnimalHippocampusLipopolysaccharidesMaleMiceMice, TransgenicNeuroinflammatory DiseasesAmyloid beta-PeptidesCCR5 Receptor AntagonistsCytokinesLipopolysaccharidesMaraviroc

Identifiers

PMID42401549
PMCPMC13616923

What OpenQuestion holds

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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.