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Clinical Aspects and Molecular Mechanisms of Cognitive Dysfunction in Children and Adolescents with Type 1 Diabetes

Bibliographic Data

ID15712738
AuthorsELENI ANGELOPOULOU (National and Kapodistrian University of Athens, corresponding author), Nicolas C Nicolaides (0000-0001-8260-1309, University of Cyprus), Alexandros Gryparis (0000-0003-0563-0282, University of Ioannina), Tania Siahanidou (0000-0001-8991-0649, National and Kapodistrian University of Athens), Panagiota Pervanidou (0000-0002-6593-6489, National and Kapodistrian University of Athens), Christina Kanaka‐Gantenbein (0000-0001-6942-6470, National and Kapodistrian University of Athens), Christina Kanaka-Gantenbein (National and Kapodistrian University of Athens)
Year2026
Volume13
Issue3
Pages416-416
Publication date2026-03-18
Peer ReviewedYes
Open AccessYes
TypeARTICLE
VenueChildren (JOURNAL)
Journal identifiersISSN: 2227-9067 • E-ISSN: 2227-9067
PublisherMultidisciplinary Digital Publishing Institute (PUBLISHER • CH)
DOI10.3390/children13030416
PMID41897128
OpenAlexW7139000149
LanguageEN
References cited91

Type 1 diabetes (T1D) constitutes a chronic metabolic disorder attributed to the autoimmune destruction of insulin-producing pancreatic β cells, which most frequently occurs in childhood. Long-term complications of T1D are expected to occur mainly in adult life, whereas cognitive dysfunction can also occur in children and adolescents with T1D. Most studies demonstrate mild cognitive impairment, especially in the domains of memory, attention and executive functions, all of which affect academic performance, which may also negatively influence adherence to appropriate glucose monitoring and insulin treatment in children and adolescents with T1D. As a result, mild cognitive dysfunction can be an obstacle to both optimal glycemic control during childhood and adolescence and academic achievements for young individuals with T1D. The major metabolic changes occurring around the onset of diabetes, such as severe hyperglycemia and diabetic ketoacidosis, may have a negative impact on brain plasticity during this vulnerable period of neurodevelopment, especially in children diagnosed at a younger age. The pathophysiological mechanisms involved are closely related to increased oxidative stress and the accumulation of advanced glycation end products in the brain, thus leading to neuron cell damage and apoptosis. On the other hand, hypoglycemic episodes and glucose fluctuations may also impair neuronal integrity. The aim of the current narrative review is therefore to present the existing literature data on the clinical aspects, risk factors and molecular mechanisms associated with cognitive dysfunction in children and adolescents with T1D

Affect (linguistics · Cognition · Diabetes mellitus · Glycation · Glycemic · Insulin · Mechanism (biology · Metabolic control analysis · Pathophysiology · Type 1 diabetes · Diabetes and associated disorders · Diabetes Management and Research · Pancreatic function and diabetes

  • Effects of Diabetic Ketoacidosis on Executive Function in Children With Type 1 Diabetes

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Citation velocityhistorical
Highly citedNo

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