posted on 2020-06-22, 20:15authored byAda AdminAda Admin, Lara C. Foland-Ross, Gabby Tong, Nelly Mauras, Allison Cato, Tandy Aye, Michael Tansey, Neil H. White, Stuart A. Weinzimer, Kimberly Englert, Hanyang Shen, Paul K. Mazaika, Allan L. Reiss, Diabetes Research in Children Network (DirecNet)
Glucose is a primary fuel source to the
brain, yet the influence of dysglycemia on neurodevelopment in children with
type 1 diabetes remains unclear. We examined brain activation using functional
MRI in 80 children with type 1 diabetes (mean age ± SD, 11.5±1.8 years; 46%
female) and 47 children without diabetes (“control”, mean age 11.8±1.5 years;
51% female) as they performed a visuospatial working memory (N-back) task. Results
indicated that in both groups, activation scaled positively with increasing
working memory load across many areas, including the frontoparietal cortex,
caudate and cerebellum. Between groups, children with diabetes exhibited reduced
performance on the N-back task relative to control children, as well as greater
modulation of activation (i.e., showed greater a increase in activation with higher
working memory load). Post-hoc analyses indicated that greater modulation was associated
in the diabetes group with better working memory function and with an earlier
age of diagnosis. These findings suggest that increased modulation may occur as
a compensatory mechanism, helping in part to preserve working memory ability,
and further, that children with an earlier onset require additional
compensation. Future studies that test whether these patterns change as a
function of improved glycemic control are warranted.
Funding
This research was supported by the National Institutes of Health Eunice Kennedy Shriver National Institute of Child Health and Human Development (DIRECNET: HD-41906, HD-41908, HD-41915, HD-41918, HD-56526, R01-HD-078463 and U54 HD087011 to the Intellectual and Developmental Disabilities Research Center at Washington University), by the Washington University Institute of Clinical and Translational Sciences grant UL1TR000448 from the National Center for Advancing Translational Sciences (NCATS) of the National Institutes of Health (NIH) and by the Stanford University grant UL1TR001085 from the National Institutes of Health (NIH) and National Center for Research Resources (NCRR).