Type 2 diabetes (T2D) is increasingly associated with cognitive impairment and dementia, reflecting the combined impact of metabolic dysregulation, vascular injury, neuroinflammation, and defective brain insulin signaling. While this link is now well recognized, it remains unclear whether cognitive decline in T2D is modifiable. This review focuses on emerging neuroprotective strategies, highlighting both pharmacological and lifestyle-based interventions. Recent evidence indicates that some glucose-lowering agents, notably metformin, sodium-glucose cotransporter 2 inhibitors, and glucagon-like peptide-1 receptor agonists, may exert pleiotropic effects on brain metabolism, inflammation, and vascular integrity beyond glycemic control. We propose a conceptual shift in T2D management in which cognitive preservation becomes an explicit therapeutic objective, integrating metabolic control with targeted brain-protective approaches.
Neuroprotective strategies for cognitive decline in type 2 diabetes / Cimini, F.A., Cuenca-Royo, A., Gomis-Gonzalez, M., Forcano, L., Barchetta, I., Barone, E., Cavallo, M.G., De La Torre, R.. - In: TRENDS IN ENDOCRINOLOGY AND METABOLISM. - ISSN 1879-3061. - (2026). [10.1016/j.tem.2026.04.003]
Neuroprotective strategies for cognitive decline in type 2 diabetes
Cimini, Flavia A;Barchetta, Ilaria;Barone, Eugenio;Cavallo, Maria G;
2026
Abstract
Type 2 diabetes (T2D) is increasingly associated with cognitive impairment and dementia, reflecting the combined impact of metabolic dysregulation, vascular injury, neuroinflammation, and defective brain insulin signaling. While this link is now well recognized, it remains unclear whether cognitive decline in T2D is modifiable. This review focuses on emerging neuroprotective strategies, highlighting both pharmacological and lifestyle-based interventions. Recent evidence indicates that some glucose-lowering agents, notably metformin, sodium-glucose cotransporter 2 inhibitors, and glucagon-like peptide-1 receptor agonists, may exert pleiotropic effects on brain metabolism, inflammation, and vascular integrity beyond glycemic control. We propose a conceptual shift in T2D management in which cognitive preservation becomes an explicit therapeutic objective, integrating metabolic control with targeted brain-protective approaches.| File | Dimensione | Formato | |
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