Evidence map›Paper›PMID 42064068›Full record

ReviewFrontiers in immunology2026

The complement system in Alzheimer's disease: mechanisms, biomarkers, and therapeutic implications.

Guokang Liu, Boshao Deng, Xiao Han, Yunpei Zhao, Shiyu Zeng, Suqin Yu, Lulu Wang, Siyi Wang, Yufei Wu, Linyuan Cai and 3 more

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 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

13 authors.

Guokang Liu *Department of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Boshao Deng *Department of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Xiao Han *Department of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Yunpei Zhao *Department of Pharmacy, Southwest Hospital, Third Military Medical University, Chongqing, China.
Shiyu ZengDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Suqin YuDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Lulu WangDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Siyi WangDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Yufei WuState Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China.
Linyuan CaiAnyue County People's Hospital, Ziyang, Sichuan, China.
Yuzhang WuDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Hong YangDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.
Jian ChenDepartment of Immunology, Army Medical University (Third Military Medical University), Chongqing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder in which synaptic loss is closely associated with cognitive decline. Although the amyloid hypothesis has long dominated AD research, the limited efficacy of amyloid-targeted therapies highlights the need to explore additional pathogenic mechanisms. Increasing evidence indicates that dysregulation of the complement system plays a critical role in AD, linking genetic risk, protein aggregation, neuroinflammation, and neurodegeneration. Under physiological conditions, complement signaling is essential for neural development and synaptic refinement; however, in AD, aberrant activation contributes to excessive synaptic pruning and sustained inflammatory responses. As a result, complement components have attracted attention as potential biomarkers and therapeutic targets, despite limitations in disease specificity. This review summarizes current advances in understanding complement system alterations in AD, discusses their roles in disease pathogenesis, and highlights emerging complement-targeted therapeutic strategies, as well as remaining challenges related to intervention timing, patient stratification, and blood-brain barrier delivery.

Indexed as

Alzheimer DiseaseComplement System ProteinsAnimalsBiomarkersBlood-Brain BarrierComplement ActivationHumansBiomarkersComplement System ProteinsAlzheimer’s diseasebiomarkerscomplement systemdisease-modifying therapyneuroinflammationsynaptic pruning

Identifiers

PMID42064068
PMCPMC13124525

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.