candidate markers for SCZ and BD [54, 56], and it has been shown that loci within the KCN family genes (i.e., KCNB2) are pleiotropic to several psychiatric disorders [14]. Interestingly, transcriptional correlations of PC1 were found enriched to the developmental stage starting from late childhood, in parallel with the onset of significant cortical thinning as well as the emergence of psychopathology. We speculate that the PC1 may reflect microstructural variation across regions, which could be supported by the supplementary findings showing significant correlations between the CT reconstructed with PC1 and cell density at both age 10 and 12 years. It is possible that the increased expression of PC1-related genes is related to the elevated cell density during this period. One hypothesis arising from the present results is that a disruption in neurotypical development related to these microstructural mechanisms contributes to the etiology of psychiatric disorders that emerge during adolescence. For instance, a previous study reported that genes associated with voltage-gated cation channels and psychiatric disorders (i.e., BD and SCZ) showed a preferentially increased expression during adolescence and early adulthood [54].
