SynthesisJournal of neural transmission (Vienna, Austria : 1996)2018
Association of CD14-260 (-159) C/T and Alzheimer's disease: systematic review and trial sequential analyses.
Synthesis in Journal of neural transmission (Vienna, Austria : 1996), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Water stress in Musa spp.: A systematic review.PloS one · 2018Pooled it
- Comparison of Extracellular Vesicles from Induced Pluripotent Stem Cell-Derived Brain Cells.International journal of molecular sciences · 2024Article
- Analysis of complement system and its related factors in Alzheimer's disease.BMC neurology · 2023Article
- Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current studies have evaluated the association between CD14-260 (also known as -159) C/T polymorphism and Alzheimer's disease (AD) susceptibility. However, the association remains inconclusive. The aim of this study was to draw an accurate conclusion of the association. The literature search was conducted using PubMed, Embase, Chinese National Knowledge Infrastructure, China Biological Medicine Database, and Wanfang Databases for related articles. Four case-control studies with a total of 868 cases and 766 controls were eligible to be included in this meta-analysis. The association was evaluated by calculating the odds ratios (ORs) with the corresponding 95% confidence intervals (CIs). Overall, there was no significant association between CD14-260C/T polymorphism and AD risk in all genetic models (the allele model T vs. C: OR = 1.06, 95% CI 0.92-1.21, p = 0.44; the homozygous model TT vs. CC: OR = 1.09, 95% CI 0.83-1.44, p = 0.53; the heterozygote model CT vs. CC: OR = 0.95, 95% CI 0.75-1.22, p = 0.71; the dominant model TT + CT vs. CC: OR = 1.05, 95% CI 0.84-1.32, p = 0.66; the recessive model TT vs. CT + CC: OR = 1.14, 95% CI 0.92-1.43, p = 0.24). The sample size of 5064 was calculated by applying trial sequential analysis. Cumulative z curve does not cross trial sequential monitoring boundary. In conclusion, the present meta-analysis suggests that the CD14-260C/T polymorphism may not be associated with genetic susceptibility of AD, but the association remains indeterminate due to the insufficient evidence.
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Registered trials
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