Published online Dec 15, 2014. doi: 10.4239/wjd.v5.i6.889
Revised: October 17, 2014
Accepted: October 31, 2014
Published online: December 15, 2014
Processing time: 123 Days and 18.3 Hours
Epidemiological and biological evidences support a link between type 2 diabetes mellitus (DM2) and Alzheimer’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 areas 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 controlling 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 cognitive dysfunction and dementia. Hypoglycemia may also have deleterious effects on cognitive function. Recurrent symptomatic and asymptomatic hypoglycemic episodes have been suggested to cause sub-clinical brain damage, and permanent cognitive impairment. Future trials are required to clarify the mechanistic link, to address the question whether cognitive decline may be prevented by an adequate metabolic control, and to elucidate the role of drugs that may cause hypoglycemic episodes.
Core tip: Epidemiological and biological evidences support a link between type 2 diabetes (DM2) and Alzheimer’s disease (AD). Persons with diabetes have increased incidence of cognitive decline and AD. Increased cortical and subcortical atrophy is present after controlling for vascular disease and inadequate cerebral circulation. Recent studies confirmed the role of insulin as possible link between DM2 and AD. Altered insulin signaling may contribute to AD biochemical and histopathological lesions. Hyperglycemia and hypoglycemia also have deleterious effects on cognitive function. Future trials would clarify the mechanistic link, and if cognitive decline may be prevented by an adequate metabolic control, and avoiding hypoglycemia.