ArticleJournal of molecular neuroscience : MN2017
Validating GWAS Variants from Microglial Genes Implicated in Alzheimer's Disease.
Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.
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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.
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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.
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Who cites it
29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.
- Systematic review and meta-analysis of the association betweenFrontiers in aging neuroscience · 2024Pooled it
- Complement receptor 1 genetic polymorphism contributes to sporadic Alzheimer's disease susceptibility in Caucasians: a meta-analysis.Bioscience reports · 2020Pooled it
- Chimeric Antigen Receptor Cell Therapy: Current Status and Its Potential in Aging and Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Coupling relationship between glucose and oxygen metabolisms to serve as an imaging biomarker for Alzheimer's disease.Scientific reports · 2025Article
- CD33 and SHP-1/Genes · 2024Article
- The Role of Changes in the Expression of Inflammation-Associated Genes in the Variants of Cerebral Small Vessel Disease.International journal of molecular sciences · 2024Article
- Alzheimer's Disease: Models and Molecular Mechanisms Informing Disease and Treatments.Bioengineering (Basel, Switzerland) · 2024Review
- Alzheimer's genes in microglia: a risk worth investigating.Molecular neurodegeneration · 2023Review
- Molecular Insights into Cell Type-specific Roles in Alzheimer's Disease: Human Induced Pluripotent Stem Cell-based Disease Modelling.Neuroscience · 2023Review
- Advances in Molecular Psychiatry - March 2023: mitochondrial function, stress, neuroinflammation - bipolar disorder, psychosis, and Alzheimer's disease.Molecular psychiatry · 2023Article
- Influence of Host Age on Intracranial AAV9 TauP301L Induced Tauopathy.Journal of Alzheimer's disease : JAD · 2023Article
- Review
- Transcriptomic Profiling Identifies CD8Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Zebrafish as a model organism for neurodegenerative disease.Frontiers in molecular neuroscience · 2022Review
- Functional insight into LOAD-associated microglial response genes.Open biology · 2022Review
- The Glymphatic System (En)during Inflammation.International journal of molecular sciences · 2021Review
- Structural Covariance Network as an Endophenotype in Alzheimer's Disease-Susceptible Single-Nucleotide Polymorphisms and the Correlations With Cognitive Outcomes.Frontiers in aging neuroscience · 2021Article
- First Report of CR1 Polymorphisms and Soluble CR1 Levels Associated with Late Onset Alzheimer's Disease (LOAD) in Latin America.Journal of molecular neuroscience : MN · 2020Article
- Shifting equilibriums in Alzheimer's disease: the complex roles of microglia in neuroinflammation, neuronal survival and neurogenesis.Neural regeneration research · 2020Review
- Does the CD33 rs3865444 Polymorphism Confer Susceptibility to Alzheimer's Disease?Journal of molecular neuroscience : MN · 2020Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Late-onset Alzheimer's disease (LOAD) is a multifactorial neurodegenerative disorder that corresponds to most Alzheimer's disease (AD) cases. Inflammation is frequently related to AD, whereas microglial cells are the major phagocytes in the brain and mediate the removal of Aβ peptides. Microglial cell dsyregulation might contribute to the formation of amyloid plaques, a hallmark of AD. Genome-wide association studies have reported genetic loci associated with the inflammatory pathway involved in AD. Among them, rs3865444 CD33, rs3764650 ABCA7, rs6656401 CR1, and rs610932 MS4A6A variants in microglial genes are associated with LOAD. These variants are proposed to participate in the clearance of Aβ peptides. However, their association with LOAD was not validated in all case-control studies. Thus, the present work aimed to assess the involvement of CD33 (rs3865444), ABCA7 (rs3764650), CR1 (rs6656401), and MS4A6A (rs610932) with LOAD in a sample from southeastern Brazil. The genotype frequencies were assessed in 79 AD patients and 145 healthy elders matched for sex and age. We found that rs3865444 CD33 acts as a protective factor against LOAD. These results support a role for the inflammatory pathway in LOAD.
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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.