ArticleGenes2021
The Impact of Complement Genes on the Risk of Late-Onset Alzheimer's Disease.
Article in Genes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 31 citations in OpenAlex.
- Modeling common Alzheimer's disease with high and low polygenic risk in human iPSC: A large-scale research resource.Stem cell reports · 2025Article
- Unique nigral and cortical pathways implicated by epigenomic and transcriptional analyses in rotenone Parkinson's model.NPJ Parkinson's disease · 2025Article
- The expression of shelterin genes and telomere repeat analysis and their effect on Alzheimer's disease.Molecular biology reports · 2024Article
- Investigating CR1 as an indicated Gene for mild cognitive impairment in type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2024Article
- Common risk alleles for schizophrenia within the major histocompatibility complex predict white matter microstructure.Translational psychiatry · 2024Article
- The complement system in neurodegenerative diseases.Clinical science (London, England : 1979) · 2024Article
- C5aR1 signaling promotes region- and age-dependent synaptic pruning in models of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- C5aR1 signaling promotes region and age dependent synaptic pruning in models of Alzheimer's Disease.bioRxiv : the preprint server for biology · 2023Article
- Is Drp1 a link between mitochondrial dysfunction and inflammation in Alzheimer's disease?Frontiers in molecular neuroscience · 2023Review
- Marine Sources of DHA-Rich Phospholipids with Anti-Alzheimer Effect.Marine drugs · 2022Review
- C5aR1 antagonism alters microglial polarization and mitigates disease progression in a mouse model of Alzheimer's disease.Acta neuropathologica communications · 2022Article
- Review
- Article
- Kurt Jellinger 90: his contribution to neuroimmunology.Journal of neural transmission (Vienna, Austria : 1996) · 2021Review
- The Role of Complement in Synaptic Pruning and Neurodegeneration.ImmunoTargets and therapy · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Late-onset Alzheimer's disease (LOAD), the most common cause of dementia, and a huge global health challenge, is a neurodegenerative disease of uncertain aetiology. To deliver effective diagnostics and therapeutics, understanding the molecular basis of the disease is essential. Contemporary large genome-wide association studies (GWAS) have identified over seventy novel genetic susceptibility loci for LOAD. Most are implicated in microglial or inflammatory pathways, bringing inflammation to the fore as a candidate pathological pathway. Among the most significant GWAS hits are three complement genes:
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.