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PNAS Papers on Neurodevelopment Risk Scores in Placenta, Ancient Human Dispersal to China, More

Editor's Note: Some of the articles described below are not yet available at the PNAS site, but they are scheduled to be posted some time this week.

A Lieber Institute for Brain Development-led team explores potential placental expression-based genomic risk scores (PlacGRS) for schizophrenia in infants with a history of prenatal or early-life complications. Based on placental gene expression and clinical data for hundreds of infants with a history of early-life complications, the team saw apparent ties between the placental neurodevelopmental risk scores and features such as neonatal brain volume or cognitive development at one year. "These negative associations are stronger in males, found only in [genomic risk scores] fractionated by placental gene expression, and not found in PlacGRS for other developmental disorders and traits," the authors report, noting that the schizophrenia score may help offer a "potentially reversible neurodevelopmental path of risk that may be unique to schizophrenia." 

Researchers from Nanjing University, Fudan University, and other centers in China, Australia, and Taiwan share findings from an ancient DNA-based analysis of samples from five caves in China. The sites included three caves in southern China where very early human habitation was proposed from prior paleoanthropology studies, along with two sites in the northern Hubei province, the team says. From their ancient mitochondrial genome analyses, coupled with multiple dating methods, the authors conclude that anatomically modern human samples found at these sites "were much younger than previously suggested, with some remains dating to the Holocene owing to the complex depositional history of these subtropical caves." Contrary to the early dispersal theory, they say, such results suggest that anatomically modern humans "settled southern China within the timeframe set by molecular data of less than [50,000 to 45,000 years ago] and no earlier." GenomeWeb has more on this, here.

A team from Taiwan and the US outline a role for the methyltransferase enzyme-coding gene METTL3 and related N6-methyladenosine RNA methylation levels in inflammatory pathways that influence the development of atherosclerosis. By profiling N6-methyladenosine RNA methylation in human umbilical vein endothelial cells and mouse aortic endothelial cells exposed to a range of conditions, including altered blood flow due to oscillatory stress, the researchers saw an oscillatory stress-related rise in methylation by METTL3 at these sites, along with altered expression of genes from downstream pathways influencing hemodynamics and atherosclerosis. "Collectively, METTL3 and [N6-methyladenosine] hypermethylation epigenetically regulates the atherogenic gene expression and phenotypes in the initiation of atherosclerosis," they write, adding that the findings. "may enlighten the field of RNA epigenetics in the pathogenic mechanisms of heart diseases."