Structural MRI yields information about brain anatomy, including gray- and white-matter volumes as well as gyrus and sulcus development, and this approach is wellsuited for studies seeking to predict future ASDs diagnoses in infants. Very briefly, the structural MRI literature indicates accelerated brain growth during earlydevelopment in ASDs.135,136 There are reports of significantly large head circumference137 and brain volume in children with autism.138 Longitudinal studies indicate that ASDs are characterized by an early transient period of postnatal brain

Inhibitors,research,lifescience,medical overgrowth evident in 70% of children with ASDs before age 2 that is not present in adolescence and adulthood.139-140 Evidence of enlarged total brain size in ASDs is accompanied by studies showing smaller cerebellar vermis,141,142 amygdala, and hippocampus.138 Increased brain size in young children with ASDs has also been linked to increased frontal lobe white matter143 followed by reduced white matter in early and late adolescence Inhibitors,research,lifescience,medical and adulthood.144,145 Olaparib nmr diffusion tensor imaging Because the contrast properties of structural MRI are suboptimal for differentiating still-myelinating white matter from surrounding gray matter in children,146

diffusion tensor imaging (DTI), a measure of microstructural properties of white matter fibers, has emerged as a valuable tool to assess white-matter structure in very young samples.147 There is evidence of widespread Inhibitors,research,lifescience,medical abnormalities in white-matter fiber tract

integrity in ASDs, but the extent and developmental course of these differences remains unclear.148-151 Inhibitors,research,lifescience,medical Two- to three-year-old children with ASDs are characterized by increased fractional anisotropy (an index of white matter fiber density) in the frontal lobes and in the corpus callosum,152 Inhibitors,research,lifescience,medical but in 5-year-old children with ASDs fractional anisotropy was reduced in frontal lobe tracts and no different from controls in tracts connecting frontal and posterior regions.153 In 10- to 18-year-old children with ASDs, there is evidence of reduced fractional anisotropy in frontal-posterior tracts154 and in hemispheric fractional anisotropy lateralization in the arcuate fasciculus,155,156 but fractional anisotropy was found Endonuclease to be reduced in adolescents with ASDs in prefrontal cortex and tempoparietal junction.157 It thus appears that young children with ASDs are characterized by increased fractional anisotropy- in brain areas mediating social communication, whereas adolescents and adults with ASDs are characterized by generally lower fractional anisotropy, a pattern that recapitulates patterns of brain overgrowth discussed earlier. Finally, a prospective DTI study of 6- to 24-month-old infants at high-risk of developing ASDs found that fractional anisotropy trajectories for 12 of 15 fiber tracts examined differed between infants who later were identified as having an ASDs and those who did not.