5/27/2023 0 Comments Mazaika 4.0![]() Conversely, energy deprivation during hypoglycemia may abet defective apoptotic processes, spur reactive gliosis, or lead to cellular necrosis via excitotoxicity of glutamate receptors ( 7, 8). More specifically, nonenzymatic glycation of neural tissue is believed to lead to increased oxidative stress during hyperglycemia ( 5), and ultimately neurodegradation, while cell death may be instigated through deficiencies in insulin-sensitive signaling pathways ( 6). Although the effects of metabolic perturbations in T1D on central nervous system structure are not fully understood, neuronal damage is generally believed to be a consequence of both hyper- and hypoglycemic states. Neuroanatomical insult from dysglycemia may be particularly consequential in early childhood, which is a period of dynamic brain development that includes rapid myelination of neurons as well as maturation, modification, and pruning of synapses ( 4). Glucose dysregulation in type 1 diabetes (T1D) can result in physiological complications, such as neuropathies ( 1), and has also been linked to an increased risk for cognitive deficits and psychological dysfunction ( 2, 3). Thus, early-onset T1D affects regions of the brain that are associated with typical cognitive development. Cognitive correlations of intelligence quotient to GMV were found in cerebellar-occipital regions and medial prefrontal cortex for control subjects, as expected, but not for the T1D group. Within the T1D group, hyperglycemic exposure was associated with decreased GMV in medial frontal and temporal-occipital regions and increased GMV in lateral prefrontal regions. Relative to control subjects, the T1D group displayed decreased gray matter volume (GMV) in bilateral occipital and cerebellar regions ( P < 0.001) and increased GMV in the left inferior prefrontal, insula, and temporal pole regions ( P = 0.002). Whole-brain volumetric analyses were conducted using voxel-based morphometry to detect regional differences between groups and to investigate correlations between regional brain volumes and measures of glycemic exposure (including data from continuous glucose monitoring). ![]() ![]() Structural magnetic resonance images of the brain were acquired in 142 children with T1D and 68 age-matched control subjects (mean age 7.0 ± 1.7 years) on six identical scanners. In this study, we investigate the neuroanatomical correlates of dysglycemia in very young children with early-onset T1D. Studies of brain structure in type 1 diabetes (T1D) describe widespread neuroanatomical differences related to exposure to glycemic dysregulation in adults and adolescents.
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