Young type 1 diabetes patients can develop several possible illness-related neuropathological processes, including gliosis, demyelination, and altered osmolarity, 12 years after diagnosis. Previously, the researchers identified neurocognitive deficits 6 years after the diagnosis of type 1 diabetes onset in youth studied prospectively from diagnosis. In the present study, they reevaluated this cohort 12 years after study inception. Neurocognitive assessment and neuroimaging were used to examine brain function in 106 youth with type 1 diabetes and 75 control subjects. Verbal (p = 0.03) and full scale IQs (p = 0.05) were lower among patients with type 1 diabetes than among controls. Compared with control subjects, those with type 1 diabetes had lower N-acetylaspartate in frontal lobes and basal ganglia and higher myoinositol and choline in frontal and temporal lobes and basal ganglia. Gray matter was decreased in bilateral thalami and right parahippocampal gyrus and insular cortex in diabetic subjects. Patients with diabetes also had decreased white matter in bilateral parahippocampi, left temporal lobe, and middle frontal area. Among diabetics, there was an increase in T2 relaxation times in left superior temporal gyrus and a decrease in bilateral lentiform nuclei, caudate nuclei and thalami, and right insular area. The investigators reported that early-onset disease was predictive of lower performance IQ and full scale IQ. An association was observed between hypoglycemia and lower verbal IQ and reduced gray matter volume in the thalamus. Poor metabolic control predicted elevated myoinositol in basal ganglia and decreased T2 in the thalamus. Older age predicted volume loss and altered T2.