Evidence map›Paper›PMID 35204837›Full record

ReviewBiomolecules2022

The Complement System in the Central Nervous System: From Neurodevelopment to Neurodegeneration.

Ying Chen, John Man Tak Chu, Raymond Chuen Chung Chang, Gordon Tin Chun Wong

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.7field-weighted citation impact, top 4% of its field
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

44 citing papers in PubMed, 66 citations in OpenAlex.

  1. Immune dysregulation and epileptogenesis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  2. Article
  3. The neuroimmune system and cognition.Nature immunology · 2026
    Review
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  8. ODC1 restricts meningeal B cell age-associated-like phenotype and function in multiple sclerosis: A human and experimental study.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  19. Redox modulation of the complement cascade contributes to synapse loss in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  20. 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

4 authors at 1 institution in 1 country.

Ying ChenDepartment of Anaesthesiology, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
John Man Tak ChuDepartment of Anaesthesiology, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.ORCID 0000-0003-2377-1054
Raymond Chuen Chung ChangLaboratory of Neurodegenerative Diseases, School of Biomedical Sciences, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.ORCID 0000-0001-8538-7993
Gordon Tin Chun WongDepartment of Anaesthesiology, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.ORCID 0000-0002-8127-4593
Chinese University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The functions of the complement system to both innate and adaptive immunity through opsonization, cell lysis, and inflammatory activities are well known. In contrast, the role of complement in the central nervous system (CNS) which extends beyond immunity, is only beginning to be recognized as important to neurodevelopment and neurodegeneration. In addition to protecting the brain against invasive pathogens, appropriate activation of the complement system is pivotal to the maintenance of normal brain function. Moreover, overactivation or dysregulation may cause synaptic dysfunction and promote excessive pro-inflammatory responses. Recent studies have provided insights into the various responses of complement components in different neurological diseases and the regulatory mechanisms involved in their pathophysiology, as well as a glimpse into targeting complement factors as a potential therapeutic modality. However, there remain significant knowledge gaps in the relationship between the complement system and different brain disorders. This review summarizes recent key findings regarding the role of different components of the complement system in health and pathology of the CNS and discusses the therapeutic potential of anti-complement strategies for the treatment of neurodegenerative conditions.

Indexed as

Central Nervous SystemNeurodegenerative DiseasesBrainComplement System ProteinsHumansComplement System Proteinsastrocytescomplementmicroglianeurodegenerationneurodevelopmentneuroinflammationneurons

Identifiers

PMID35204837
PMCPMC8869249
OpenAlexW4213081684

What Socratic holds

Textmetadata
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 Socratic graph.