ReviewMolecular neurobiology2015
CR1 in Alzheimer's disease.
Review in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 6 of them syntheses that pooled 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.
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
52 citing papers in PubMed, 6 syntheses or guidelines pooled it, 89 citations in OpenAlex.
- Dissecting the genetic and proteomic risk factors for delirium.Nature aging · 2026Pooled it
- A Multi-Ancestry GWAS Meta-Analysis Integrated with In-Depth Silico, Systems Biology, and Pharmacogenomics Approaches on Alzheimer's Disease Among 1,198,689 Subjects.Journal of molecular neuroscience : MN · 2025Pooled it
- Systematic Review on Neurotoxic Implications of Lead-Induced Gene Expression Alterations in the Etiology of Alzheimer's Disease.Cellular and molecular neurobiology · 2025Pooled it
- The role of genetic polymorphisms on drug response in Alzheimer's disease: a systematic review.BMC medical genomics · 2025Pooled it
- Genome-wide meta-analysis for Alzheimer's disease cerebrospinal fluid biomarkers.Acta neuropathologica · 2022Pooled it
- Genetic Variability in Molecular Pathways Implicated in Alzheimer's Disease: A Comprehensive Review.Frontiers in aging neuroscience · 2021Pooled it
- A Multi-Context Regulome-Wide Association Atlas for Genetic Studies of Aging Brain Disorders.medRxiv : the preprint server for health sciences · 2026Article
- Can Nutrition Modulate the Progression of Alzheimer's Disease? A Narrative Review.Current nutrition reports · 2026Review
- scTWAS: a powerful statistical framework for single-cell transcriptome-wide association studies.Nature communications · 2026Article
- Tailoring treatments: pharmacogenomics in the management of neurodegenerative diseases.Acta neurologica Belgica · 2026Review
- Immunological drivers and potential novel drug targets for major psychiatric, neurodevelopmental, and neurodegenerative conditions.Molecular psychiatry · 2025Article
- scTWAS: A powerful statistical framework for single-cell transcriptome-wide association studies.Research square · 2025Article
- Complement Cascades and Brain Disorders.Biomolecules · 2025Review
- Recent Advances and Future Directions in Alzheimer's Disease Genetic Research.International journal of molecular sciences · 2025Review
- Glial Cells in Alzheimer's Disease: Pathogenic Mechanisms and Therapeutic Frontiers.Journal of molecular neuroscience : MN · 2025Review
- Novel early-onset Alzheimer-associated genes influence risk through dysregulation of glutamate, immune activation, and intracellular signaling pathways.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- A multivariable cis-Mendelian randomization method robust to weak instrument bias and horizontal pleiotropy bias.Briefings in bioinformatics · 2025Article
- Article
- Untangling the Genetic Threads of Alzheimer's: Insights into Risk Factors and Biomarkers.Current gene therapy · 2025Review
- Identification and Validation of Potential Biomarkers and Therapeutic Targets of COVID-19-related Depression.Combinatorial chemistry & high throughput screening · 2025Article
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement component receptor 1 gene (CR1), which encodes a type-I transmembrane glycoprotein, has recently been identified as one of the most important risk genes for late-onset Alzheimer's disease (LOAD). In this article, we reviewed the recent evidence concerning the role of CR1 in LOAD. First, we introduced the structure, localization and physiological function of CR1 in humans. Afterward, we summarized the relation of CR1 polymorphisms with LOAD risk. Finally, we discussed the possible impact of CR1 on the pathogenesis of AD including amyloid-β pathology, tauopathy, immune dysfunction and glial-mediated neuroinflammation. We hope that a more comprehensive understanding of the role that CR1 played in AD may lead to the development of novel therapeutics for the prevention and treatment 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.