ReviewGenes2021
Genetic Insights into the Impact of Complement in Alzheimer's Disease.
Review in Genes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
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
19 citing papers in PubMed, 25 citations in OpenAlex.
- The complement system in Alzheimer's disease: evaluating biomarker potential in a complex neuroimmune context.Journal of neuroinflammation · 2026Review
- The Arp2/3 complex is required for in situ haptotactic response of microglia to iC3b.EMBO reports · 2026Article
- Circulating C-reactive protein influences polygenic risk of inflammatory genes expressed in brain endothelia for Alzheimer's disease.Neurobiology of disease · 2026Article
- PreoperativeFrontiers in bioinformatics · 2026Review
- The complement cascade in Alzheimer's disease: modern implications of an ancient immune protagonist.Molecular neurodegeneration · 2025Review
- The Alzheimer's disease-associated complement receptor 1 variant confers risk by impacting glial phagocytosis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Genetically Proxied Phosphodiesterase Type 5 (PDE5) Inhibition and Risk of Dementia: A Drug Target Mendelian Randomization Study.Molecular neurobiology · 2025Article
- The Association between the rs6656401 Locus of the CR1 Gene and Structural Alterations of Brain Effects in Han Chinese Patients with Alzheimer's Disease.Current Alzheimer research · 2025Article
- Single cell transcriptomes and multiscale networks from persons with and without Alzheimer's disease.Nature communications · 2024Article
- The complement system in neurodegenerative diseases.Clinical science (London, England : 1979) · 2024Article
- Factor H's Control of Complement Activation Emerges as a Significant and Promising Therapeutic Target for Alzheimer's Disease Treatment.International journal of molecular sciences · 2024Article
- A guide to complement biology, pathology and therapeutic opportunity.Nature reviews. Immunology · 2024Review
- The role of natural flavonoids on neuroinflammation as a therapeutic target for Alzheimer's disease: a narrative review.Neural regeneration research · 2023Review
- Can Genetic Markers Predict the Sporadic Form of Alzheimer's Disease? An Updated Review on Genetic Peripheral Markers.International journal of molecular sciences · 2023Review
- Article
- C3-dependent effector functions of complement.Immunological reviews · 2023Review
- Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation.Frontiers in human neuroscience · 2023Article
- The impact of increasing levels of blood C-reactive protein on the inflammatory loci SPI1 and CD33 in Alzheimer's disease.Translational psychiatry · 2022Article
- C5aR1 antagonism alters microglial polarization and mitigates disease progression in a mouse model of Alzheimer's disease.Acta neuropathologica communications · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The presence of complement activation products at sites of pathology in post-mortem Alzheimer's disease (AD) brains is well known. Recent evidence from genome-wide association studies (GWAS), combined with the demonstration that complement activation is pivotal in synapse loss in AD, strongly implicates complement in disease aetiology. Genetic variations in complement genes are widespread. While most variants individually have only minor effects on complement homeostasis, the combined effects of variants in multiple complement genes, referred to as the "complotype", can have major effects. In some diseases, the complotype highlights specific parts of the complement pathway involved in disease, thereby pointing towards a mechanism; however, this is not the case with AD. Here we review the complement GWAS hits;
Indexed as
Identifiers
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.