Sports-related concussion in adolescents is a major public health issue; however, little is known about the underlying changes in functional brain connectivity. We evaluated connectivity of resting-state brain networks to determine whether alterations in specific networks distinguish adolescents with sports-related concussion from a group of healthy, active control adolescents. Twelve adolescents with a clinical diagnosis of subacute concussion and ten healthy adolescents matched for age, gender, and physical activity completed functional magnetic resonance imaging (fMRI) scanning. Functional connectivity of resting-state brain networks was evaluated in both groups using probabilistic independent component analysis (ICA). Altered functional connectivity was found within three resting-state networks in adolescents with concussion. Specifically, we noted: a) alterations within the default mode network; b) increased connectivity in the right frontal pole in the executive function network; and c) increased connectivity in the left frontal operculum cortex associated with the ventral attention network. This preliminary report shows that whole-brain functional connectivity is altered in networks related to cognition and attention in adolescents in the subacute phase following sports-related concussion. This first report in adolescents should be used to inform future studies in larger cohorts of adolescents with sports-related concussion. Increased knowledge of these changes may lead to improvements in clinical management and help to develop rehabilitation programs.

Background: The presence of an extra whole or part of chromosome 21 in people with Down syndrome (DS) is associated with multiple neurological changes, including pathological aging that often meets the criteria for Alzheimer’s Disease (AD). In addition, trisomies have been shown to disrupt normal epigenetic marks across the genome, perhaps in response to changes in gene dosage. We hypothesized that trisomy 21 would result in global epigenetic changes across all participants, and that DS patients with cognitive impairment would show an additional epigenetic signature. Methods: We therefore examined whole-genome DNA methylation in buccal epithelial cells of 10 adults with DS and 10 controls to determine whether patterns of DNA methylation were correlated with DS and/or cognitive impairment. In addition we examined DNA methylation at the APP gene itself, to see whether there were changes in DNA methylation in this population. Using the Illumina Infinium 450 K Human Methylation Array, we examined more than 485,000 CpG sites distributed across the genome in buccal epithelial cells. Results: We found 3300 CpGs to be differentially methylated between the groups, including 495 CpGs that overlap with clusters of differentially methylated probes. In addition, we found 5 probes that were correlated with cognitive function including two probes in the TSC2 gene that has previously been associated with Alzheimer’s disease pathology. We found no enrichment on chromosome 21 in either case, and targeted analysis of the APP gene revealed weak evidence for epigenetic impacts related to the AD phenotype. Conclusions: Overall, our results indicated that both Trisomy 21 and cognitive impairment were associated with distinct patterns of DNA methylation.