2015 Volume 26 Issue 2 Pages 129-134
Diabetes, a risk factor for cerebral infarction, increases the risk of vascular dementia by 2.0–4.2 times and that of Alzheimer disease by 1.1–2.4 times. Mechanisms include cerebral ischemia induced by atherosclerosis, white matter lesion caused by small vessel disease, impaired amyloid clearance, glucose toxicity generated with advanced glycation endproducts, and hyperinsulinemia. Amyloid PET, developed recently, was used to assess amyloid loading even before the damage of the neurons. In healthy volunteers without subjective and objective higher cortical dysfunction, age-dependent accumulation of amyloid was observed, showing high amyloid loading in the elderly. The diabetic patients with Alzheimer-type dementia showed no specific accumulation pattern in amyloid. Diabetes may just facilitate amyloid toxicity without diabetes-specific process. Recently amyloid clearance was reported to decrease in Alzheimer disease, especially in cases with white matter lesions. Impaired blood-brain barrier in these cases may reduce amyloid clearance from brain parenchyma. Specific treatments targeting these mechanisms may help decrease the risk for Alzheimer disease in the near future.