SynthesisJournal of neurology, neurosurgery, and psychiatry2016
Candidate-gene analysis of white matter hyperintensities on neuroimaging.
Synthesis in Journal of neurology, neurosurgery, and psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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
11 citing papers in PubMed.
- Prospective study of primary aldosteronism in acute ischemic stroke: association with small vessel disease.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- Connectomic-genetic signatures in the cerebral small vessel disease.Neurobiology of disease · 2022Article
- Article
- Emerging insights from the genetics of cerebral small-vessel disease.Annals of the New York Academy of Sciences · 2020Review
- NicotinamideInternational journal of tryptophan research : IJTR · 2020Review
- Article
- The Associations ofFrontiers in genetics · 2019Article
- Is antiplatelet treatment effective at attenuating the progression of white matter hyperintensities?PloS one · 2017Article
- Association of MTHFR C677T Genotype With Ischemic Stroke Is Confined to Cerebral Small Vessel Disease Subtype.Stroke · 2016Article
- Homocysteine Level Is Associated with White Matter Hyperintensity Locations in Patients with Acute Ischemic Stroke.PloS one · 2015Article
- Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWhite matter hyperintensities (WMH) are a common radiographic finding and may be a useful endophenotype for small vessel diseases. Given high heritability of WMH, we hypothesised that certain genotypes may predispose individuals to these lesions and consequently, to an increased risk of stroke, dementia and death. We performed a meta-analysis of studies investigating candidate genes and WMH to elucidate the genetic susceptibility to WMH and tested associated variants in a new independent WMH cohort. We assessed a causal relationship of WMH to methylene tetrahydrofolate reductase (MTHFR).
methodsDatabase searches through March 2014 were undertaken and studies investigating candidate genes in WMH were assessed. Associated variants were tested in a new independent ischaemic cohort of 1202 WMH patients. Mendelian randomization was undertaken to assess a causal relationship between WMH and MTHFR.
resultsWe identified 43 case-control studies interrogating eight polymorphisms in seven genes covering 6,314 WMH cases and 15,461 controls. Fixed-effects meta-analysis found that the C-allele containing genotypes of the aldosterone synthase CYP11B2 T(-344)C gene polymorphism were associated with a decreased risk of WMH (OR=0.61; 95% CI, 0.44 to 0.84; p=0.003). Using mendelian randomisation the association among MTHFR C677T, homocysteine levels and WMH, approached, but did not reach, significance (expected OR=1.75; 95% CI, 0.90-3.41; observed OR=1.68; 95% CI, 0.97-2.94). Neither CYP11B2 T(-344)C nor MTHFR C677T were significantly associated when tested in a new independent cohort of 1202 patients with WMH.
conclusionsThere is a genetic basis to WMH but anonymous genome wide and exome studies are more likely to provide novel loci of interest.
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