The World Health Organization (WHO) stated in March 2016 that there was scientific consensus that the mosquito-borne Zika virus was a cause of the neurological disorder Guillain–Barré syndrome (GBS) and of microcephaly and other congenital brain abnormalities based on rapid evidence assessments. Decisions about causality require systematic assessment to guide public health actions.

Zika virus (ZIKV) can cross the placental barrier, resulting in infection of the fetal brain and neurological defects including microcephaly. The cellular tropism of ZIKV and the identity of attachment factors used by the virus to gain access to key cell types involved in pathogenesis are under intense investigation. Initial studies suggested that ZIKV preferentially targets neural progenitor cells (NPCs), providing an explanation for the developmental phenotypes observed in some pregnancies.

This review highlights clinical features of the increasing cases of acute flaccid paralysis associated with anterior myelitis noted in the United States from 2012 to 2015.

Much has been written recently regarding Zika virus in pregnancy and the increased risk of microcephaly in fetuses exposed to the virus. The outbreak of infection in Brazil, especially in the northeast part of the country, has been of particular concern. The virus has been found in the fluids of pregnant mothers and during autopsy in the brains of neonates with microcephaly. Much of the concern in the media regarding the teratogenicity of Zika virus infection has focused on brain findings of microcephaly.

Common mechanisms in aging and obesity are hypothesized to increase susceptibility to neurodegeneration, however direct evidence in support of this hypothesis is lacking. We therefore performed a cross-sectional analysis of MRI-based brain structure on a population-based cohort of healthy adults. Study participants were originally part of the Cambridge Centre for Ageing and Neuroscience (Cam-CAN) and included 527 individuals aged 20 – 87 years. Cortical reconstruction techniques were used to generate measures of whole brain cerebral white matter volume, cortical thickness and surface area.

A high-resolution gene expression atlas of prenatal and postnatal brain development of rhesus monkey charts global transcriptional dynamics in relation to brain maturation, while comparative analysis reveals human-specific gene trajectories; candidate risk genes associated with human neurodevelopmental disorders tend to be co-expressed in disease-specific patterns in the developing monkey neocortex.

Studies in children and adolescents have associated early developmental manganese (Mn) exposure with inattention, impulsivity, hyperactivity, and oppositional behaviors, but causal inferences are precluded by the correlational nature of the data and generally limited control for potential confounders.

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Little is known about the influence of environmental factors on the etiology of childhood brain tumors. Researchers examined risks for brain tumors in children after prenatal and infant exposure to monitored ambient air toxics.

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Early life environments induce long-term changes in neurocognitive development and behaviour. In animal models, early environmental cues affect neuropsychological phenotypes via epigenetic processes but, as yet, there is little direct evidence for such mechanisms in humans. The researchers examined the relation between DNA methylation at birth and child neuropsychological outcomes in two culturally diverse populations using a genome-wide methylation analysis and validation by pyrosequencing.

Rodent models for urban air pollution show consistent induction of inflammatory responses in major brain regions. However, the initial impact of air pollution particulate material on olfactory gateways has not been reported. The researchers evaluated the olfactory neuroepithelium (OE) and brain regional responses to a nano-sized subfraction of urban traffic ultrafine particulate matter (nPM, < 200 nm) in vivo, ex vivo and in vitro.

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