ArticleNeuromolecular medicine2016
Genetic Factors Affecting Late-Onset Alzheimer's Disease Susceptibility.
Article in Neuromolecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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.
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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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Analyzing 74,248 Samples Confirms the Association Between CLU rs11136000 Polymorphism and Alzheimer's Disease in Caucasian But Not Chinese population.Scientific reports · 2018Pooled it
- Redirecting microglia phenotype via inhibition of NFAT1 ameliorates deficits in mouse model of synucleinopathies.Experimental & molecular medicine · 2025Article
- Dendrimers: Patents for Alzheimer's Disease.Recent patents on nanotechnology · 2025Review
- Gene expression patterns of CRYM and SIGLEC10 in Alzheimer's disease: potential early diagnostic indicators.Molecular biology reports · 2024Article
- Repercussion of Primary Nucleation Pathway: Dementia and Cognitive Impairment.Current aging science · 2024Review
- A global view of the genetic basis of Alzheimer disease.Nature reviews. Neurology · 2023Review
- Role of Chemokines in the Development and Progression of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2022Review
- Review
- A Genome-Wide Study of Single-Nucleotide Polymorphisms in MicroRNAs and Further In Silico Analysis Reveals Their Putative Role in Susceptibility to Late-Onset Alzheimer's Disease.Molecular neurobiology · 2021Article
- Alzheimer's disease risk geneeLife · 2020Article
- Association of MS4A6A, CD33, and TREM2 gene polymorphisms with the late-onset Alzheimer's disease.BioImpacts : BI · 2019Article
- Cell Type Specific Expression of Toll-Like Receptors in Human Brains and Implications in Alzheimer's Disease.BioMed research international · 2019Review
- Role of Microglia TLRs in Neurodegeneration.Frontiers in cellular neuroscience · 2018Article
- Neocortical and hippocampal TREM2 protein levels during the progression of Alzheimer's disease.Neurobiology of aging · 2017Article
- Clearance of cerebral Aβ in Alzheimer's disease: reassessing the role of microglia and monocytes.Cellular and molecular life sciences : CMLS · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease is considered a progressive brain disease in the older population. Late-onset Alzheimer's disease (LOAD) as a multifactorial dementia has a polygenic inheritance. Age, environment, and lifestyle along with a growing number of genetic factors have been reported as risk factors for LOAD. Our aim was to present results of LOAD association studies that have been done in northwestern Iran, and we also explored possible interactions with apolipoprotein E (APOE) status. We re-evaluated the association of these markers in dominant, recessive, and additive models. In all, 160 LOAD and 163 healthy control subjects of Azeri Turkish ethnicity were studied. The Chi-square test with Yates' correction and Fisher's exact test were used for statistical analysis. A Bonferroni-corrected p value, based on the number of statistical tests, was considered significant. Our results confirmed that chemokine receptor type 2 (CCR2), estrogen receptor 1 (ESR1), toll-like receptor 2 (TLR2), tumor necrosis factor alpha (TNF α), APOE, bridging integrator 1 (BIN1), and phosphatidylinositol-binding clathrin assembly protein (PICALM) are LOAD susceptibility loci in Azeri Turk ancestry populations. Among them, variants of CCR2, ESR1, TNF α, and APOE revealed associations in three different genetic models. After adjusting for APOE, the association (both allelic and genotypic) with CCR2, BIN1, and ESRα (PvuII) was evident only among subjects without the APOE ε4, whereas the association with CCR5, without Bonferroni correction, was significant only among subjects carrying the APOE ε4 allele. This result is an evidence of a synergistic and antagonistic effect of APOE on variant associations with 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 Socratic graph.