Abstract

Diabetes-induced encephalopathy has been gradually getting more attention. Recently, we read with great interest the article entitled ‘Comparative Study of Cholinergic and Oxidative Stress Biomarkers in Brains of Diabetic and Hypercholesterolemic Rats’, 1 in which the authors concluded that diabetes has a deleterious effect on the brain function, which is likely attributed to the activation of oxidative stress. We totally agree with this conclusion, and in this letter, we would like to propose that disturbance of autophagic pathway would also be involved in this pathogenesis.
Accumulating evidence shows that diabetes could cause a series of central nervous system disorders, such as cognitive impairment, depression and so on. 2 Pangare and Makino 3 have demonstrated that autophagy disturbance would contribute to the pathogenesis of diabetes. A study performed by Wei et al. 4 suggests that beclin-1, a biomarker for autophagy, was significantly decreased in the brain of diabetic rodent. Our previous study reported that 3-methyladenine, an autophagic inhibitor, attenuates therapeutic effects of sirolimus on scopolamine-induced cognitive dysfunction in a rat model. 5 The results suggested that activation of autophagic pathway exerts a beneficial effect for the cognitive dysfunction. Collectively, we proposed a hypothesis that disturbance of the autophagic pathway may be involved in the diabetes-induced oxidative response in brain.
