ReviewInternational journal of molecular sciences2024
The Importance of Complement-Mediated Immune Signaling in Alzheimer's Disease Pathogenesis.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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.
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.
Who cites it
44 citing papers in PubMed, 56 citations in OpenAlex.
- Amyloid-Related Imaging Abnormalities (ARIA) in Clinical Trials of Gantenerumab in Early Alzheimer Disease.JAMA neurology · 2025Trial
- Direct Quantification of Complement Biomarkers Using Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS).ACS pharmacology & translational science · 2026Article
- Baseline cerebrospinal fluid complement balance is associated with longitudinal memory decline in relation to plasma p‑tau181 levels in mild cognitive impairment.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Fat on Fire: Disrupted Microglial Lipid Metabolism as a Driver of Anesthetic Neurotoxicity.Neuroscience bulletin · 2026Review
- Anti-Alpha-Gal Antibodies Against Gangliosides: Preliminary Data on a New Autoimmune Target in Alzheimer's Disease Patients.International journal of molecular sciences · 2026Article
- The Role of Genetic Alterations in the Emergence of Alzheimer's Disease in Down Syndrome: A Review.The European journal of neuroscience · 2026Review
- Early binding of anti-amyloid antibodies to CAA drives complement activation, inflammation and ARIA in mice.Molecular neurodegeneration · 2026Article
- The complement system in Alzheimer's disease: evaluating biomarker potential in a complex neuroimmune context.Journal of neuroinflammation · 2026Review
- Microglia-Mediated Dysfunction of PKCγ Interneurons Underlies the Mechanical Hypersensitivity in Autism.Molecular neurobiology · 2026Article
- TNF inhibition differentially impacts regional Abeta immunotherapy efficacy in the humanized hAbAlzheimer's research & therapy · 2026Article
- Early Binding of Anti-Amyloid Antibodies to CAA Drives Complement Activation, Inflammation and ARIA in Mice.bioRxiv : the preprint server for biology · 2026Article
- Plasma Proteomic Analysis ofmedRxiv : the preprint server for health sciences · 2026Article
- Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026Review
- Integrative Analysis of Intestinal Transcriptomes UnderscoresBioinformatics and biology insights · 2026Article
- C3 lowering in adult APP KI mice rescues synapses and spares cognitive decline.Molecular neurodegeneration advances · 2026Article
- PreoperativeFrontiers in bioinformatics · 2026Review
- From Monoamines to Systems Psychiatry: Rewiring Depression Science and Care (1960s-2025).Biomedicines · 2025Article
- The complement cascade in Alzheimer's disease: modern implications of an ancient immune protagonist.Molecular neurodegeneration · 2025Review
- Orthobiologics and Peptide Therapy for Central Nervous System Repair in Neurodegenerative Conditions.Cells · 2025Review
- Longitudinal plasma proteomics: relation to incident Alzheimer's disease dementia and biomarkers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
As an essential component of our innate immune system, the complement system is responsible for our defense against pathogens. The complement cascade has complex roles in the central nervous system (CNS), most of what we know about it stems from its role in brain development. However, in recent years, numerous reports have implicated the classical complement cascade in both brain development and decline. More specifically, complement dysfunction has been implicated in neurodegenerative disorders, such as Alzheimer's disease (AD), which is the most common form of dementia. Synapse loss is one of the main pathological hallmarks of AD and correlates with memory impairment. Throughout the course of AD progression, synapses are tagged with complement proteins and are consequently removed by microglia that express complement receptors. Notably, astrocytes are also capable of secreting signals that induce the expression of complement proteins in the CNS. Both astrocytes and microglia are implicated in neuroinflammation, another hallmark of AD pathogenesis. In this review, we provide an overview of previously known and newly established roles for the complement cascade in the CNS and we explore how complement interactions with microglia, astrocytes, and other risk factors such as TREM2 and ApoE4 modulate the processes of neurodegeneration in both amyloid and tau models of AD.
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What OpenQuestion holds
Registered trials
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.