Making Connections in the Teenage Brain

2017-05-19T15:46:38Z (GMT) by Kirstie Whitaker
<p>Talk as part of Society of Biological Psychiatry annual meeting on Networks and complexity in biology, brain and behaviour.</p><p>Part of Network Architectures of the Healthy Brain as Constraints for the Spatiotemporal Patterning of Disease symposium.</p><p><br></p><p>BACKGROUND Adolescence is a period of human brain growth and high incidence of mental health disorders. The Neuroscience in Psychiatry Network (<a href="http://nspn.org.uk/">http://nspn.org.uk</a>) seeks to understand biological underpinnings of the adolescent risk of depression and schizophrenia.</p> <p>METHODS Multi-parametric mapping magnetic resonance imaging was used to measure cortical thickness and intracortical myelination in 297 population volunteers aged 14–24 years old. Regional measures at 308 locations across cortex were combined into a structural covariance network and calculated topological measures of degree and closeness centrality extracted. We related nodal measures to regional gene transcriptome data provided by the Allen Institute for Brain Science (<a href="http://human.brain-map.org/">http://human.brain-map.org</a>). All statistical analyses were conducted using permutation tests with significance set at P < .05 after correction for multiple comparisons.</p> <p>RESULTS We found that association cortical areas were thicker and less myelinated than primary cortical areas at 14 years. However, association cortex had faster rates of shrinkage and myelination over the course of adolescence. Adolescent cortical myelination and shrinkage were coupled and specifically associated with a dorsoventrally patterned gene expression profile enriched for synaptic, oligodendroglial- and schizophrenia-related genes. Topologically efficient and biologically expensive hubs of the brain anatomical network had greater rates of shrinkage/myelination and were associated with overexpression of the same transcriptional profile as cortical consolidation. All results replicated in two independent cohorts.</p> <p>CONCLUSIONS We conclude that normative human brain maturation involves a genetically patterned process of consolidating anatomical network hubs. We argue that developmental variation of this consolidation process may be relevant both to normal cognitive and behavioral changes and the high incidence of schizophrenia during human brain adolescence.</p>