Epidemiological and biological evidences support a link between type 2 diabetes mellitus (DM2) and Al-zheimer’s disease (AD). Persons with diabetes have a higher incidence of cognitive decline and an increased risk of developing all types of dementia. Cognitive deficits in persons with diabetes mainly affect the ar-eas of psychomotor efficiency, attention, learning and memory, mental flexibility and speed, and executive function. The strong epidemiological association has suggested the existence of a physiopathological link. The determinants of the accelerated cognitive decline in DM2, however, are less clear. Increased cortical and subcortical atrophy have been evidenced after con-trolling for diabetic vascular disease and inadequate cerebral circulation. Most recent studies have focused on the role of insulin and insulin resistance as possible links between diabetes and AD. Disturbances in brain insulin signaling mechanisms may contribute to the molecular, biochemical, and histopathological lesions in AD. Hyperglycemia itself is a risk factor for cogni-tive dysfunction and dementia. Hypoglycemia may also have deleterious effects on cognitive function. Recur-rent symptomatic and asymptomatic hypoglycemic epi-sodes have been suggested to cause sub-clinical brain damage, and permanent cognitive impairment. Future trials are required to clarify the mechanistic link, to ad-dress the question whether cognitive decline may be prevented by an adequate metabolic control, and to elucidate the role of drugs that may cause hypoglyce-mic episodes.
|Numero di pagine||5|
|Rivista||World Journal of Diabetes|
|Stato di pubblicazione||Published - 2014|