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Gibbard, W. B.

Publications and source records attributed to Gibbard, W. B..

2 recordsLinked to original sources

Altered markers of brain metabolism and excitability are associated with executive functioning in young children exposed to alcohol in utero

Prenatal alcohol exposure (PAE) is the leading known cause of birth defects and cognitive disabilities, with impacts on brain development and executive functioning. Abnormalities in structural and functional brain features are well-documented in children with PAE, but the effects of PAE on brain metabolism in children have received less attention. Levels of brain metabolites can be measured non-invasively using magnetic resonance spectroscopy (MRS). Here, we present the first study of PAE-related brain metabolite differences in early childhood (ages 3-8 years) and their associations with cognitive performance, including executive functioning (EF) and pre-reading skills. We measured metabolites in two cohorts of children with PAE and unexposed children using MRS in the anterior cingulate cortex (ACC; cohort 1) and left temporo-parietal cortex (LTP; cohort 2). Total choline (tCho), a marker of membrane/myelin metabolism, was elevated in both regions in children with PAE compared to unexposed children, and glutamate+glutamine (Glx), a marker of excitability, was elevated in the ACC. The PAE group exhibited more difficulties with EF, and higher tCho was associated with better EF in both PAE and unexposed groups. In addition, elevated Glx in the ACC was associated with poorer inhibitory control within the PAE group only. LTP metabolites were not significantly associated with pre-reading skills in PAE or unexposed groups. Together, these findings point to altered membrane metabolism and excitability in young children with PAE. These findings provide new insight to potential mechanisms by which PAE disrupts brain development and cognitive functioning in early childhood.

neuroscience↗

White Matter Alterations in Young Children with Prenatal Alcohol Exposure

Prenatal alcohol exposure (PAE) can lead to cognitive, behavioural, and social-emotional challenges. Previous neuroimaging research has identified alterations to brain structure in newborns, older children, adolescents, and adults with PAE; however, little is known about brain structure in young children. Extensive brain development takes place during early childhood; therefore, understanding the neurological profiles of young children with PAE is critical for early identification and effective intervention. We studied 54 children (5.21{+/-}1.11 years; 27 males) with confirmed PAE compared to 54 age- and sex-matched children without PAE. Children underwent diffusion tensor imaging between 2 and 7 years of age. Mean fractional anisotropy (FA) and mean diffusivity (MD) were obtained for 10 major white matter tracts, along with tract volume, axial and radial diffusivity (AD, RD). A univariate analysis of covariance was conducted to test for group differences (PAE vs. control) controlling for age, sex and tract volume. Our results reveal white matter microstructural differences between young children with PAE and unexposed controls. The PAE group had higher FA and/or lower MD (as well as lower AD and RD) in the genu and the body of the corpus callosum, as well as the bilateral uncinate fasciculus and pyramidal tracts. Our findings align with studies of newborns with PAE finding lower AD, but contrast those in older populations with PAE, which consistently report lower FA and higher MD. These findings may reflect premature development of white matter that may then plateau too early, leading to the lower FA/higher MD observed at older ages.

neuroscience↗