Blood-based epigenome-wide analyses of cognitive abilities.

Background: Blood-based markers of cognitive functioning might provide an accessible way to track neurodegeneration years prior to clinical manifestation of cognitive impairment and dementia.

Results: Using blood-based epigenome-wide analyses of general cognitive function, we show that individual differences in DNA methylation (DNAm) explain 35.0% of the variance in general cognitive function (g).

Probabilistic inference of the genetic architecture underlying functional enrichment of complex traits.

We develop a Bayesian model (BayesRR-RC) that provides robust SNP-heritability estimation, an alternative to marker discovery, and accurate genomic prediction, taking 22 seconds per iteration to estimate 8.4 million SNP-effects and 78 SNP-heritability parameters in the UK Biobank. We find that only ≤10% of the genetic variation captured for height, body mass index, cardiovascular disease, and type 2 diabetes is attributable to proximal regulatory regions within 10kb upstream of genes, while 12-25% is attributed to coding regions, 32-44% to introns, and 22-28% to distal 10-500kb upstream regions.

Propensity to intentional and unintentional mind-wandering differs in arousal and executive vigilance tasks.

We typically observe a decrement in vigilance with time-on-task, which favors the propensity for mind-wandering, i.e., the shifting of attention from the task at hand to task-unrelated thoughts.

Author Correction: Bayesian reassessment of the epigenetic architecture of complex traits.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Integrating transcriptional activity in genome-scale models of metabolism.

Background: Genome-scale metabolic models provide an opportunity for rational approaches to studies of the different reactions taking place inside the cell. The integration of these models with gene regulatory networks is a hot topic in systems biology. The methods developed to date focus mostly on resolving the metabolic elements and use fairly straightforward approaches to assess the impact of genome expression on the metabolic phenotype.

[Genetic thrombophilia and markers of endothelial activation in patients with preeclampsia].

Background: The presence of thrombosis in preeclampsia suggests that endothelial function could play an important role in its pathogenesis.

Objective: Determine the association between markers of genetic thrombophilia, endothelial activation and preeclampsia.

Material And Method: Prospective study of cases and controls to determine the factor V Leiden existence, protrombin G20210A, methylenetetrahydrofolate reductase C677T, activated protein C resistance and levels of von Willebrand factor and the sFlt1 receptor were determined in 28 women with preeclampsia and 41 pregnant controls.