Table of Contents Author Guidelines Submit a Manuscript
Journal of Diabetes Research
Volume 2015 (2015), Article ID 703512, 9 pages
Research Article

Type 1 Diabetes Modifies Brain Activation in Young Patients While Performing Visuospatial Working Memory Tasks

1Instituto de Neurociencias, Universidad de Guadalajara, Francisco de Quevedo 180, Colonia Arcos Vallarta, 44130 Guadalajara, JAL, Mexico
2Facultad de Psicología, Universidad Michoacana de San Nicolás de Hidalgo, Francisco Villa 450, 58120 Morelia, MICH, Mexico
3Facultat de Psicologia, Universitat de Barcelona, Institut de Recerca en Cervell, Cognició i Conducta (IR3C), Passeig de la Vall d’Hebron 171, 08035 Barcelona, Spain

Received 13 May 2015; Revised 30 June 2015; Accepted 1 July 2015

Academic Editor: Paolo Fiorina

Copyright © 2015 Geisa B. Gallardo-Moreno et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


In recent years, increasing attention has been paid to the effects of Type 1 Diabetes (T1D) on cognitive functions. T1D onset usually occurs during childhood, so it is possible that the brain could be affected during neurodevelopment. We selected young patients of normal intelligence with T1D onset during neurodevelopment, no complications from diabetes, and adequate glycemic control. The purpose of this study was to compare the neural BOLD activation pattern in a group of patients with T1D versus healthy control subjects while performing a visuospatial working memory task. Sixteen patients and 16 matched healthy control subjects participated. There was no significant statistical difference in behavioral performance between the groups, but, in accordance with our hypothesis, results showed distinct brain activation patterns. Control subjects presented the expected activations related to the task, whereas the patients had greater activation in the prefrontal inferior cortex, basal ganglia, posterior cerebellum, and substantia nigra. These different patterns could be due to compensation mechanisms that allow them to maintain a behavioral performance similar to that of control subjects.