Alzheimers disease (AD) is the most common age-related neurodegenerative disorder and cause of dementia in the elderly, characterized by global cognitive impairment and the presence of extracellular beta-amyloid (Aβ) deposition (senile plaques) and intracellular hyperphosphorylated tau protein (neurofibrillary tangles).Currently, the dominant theory to explain pathogenesis of AD is the "Amyloid Cascade Hypothesis" first proposed in 1992.However, almost all previous clinical trials targeting Aβ have received negative results.This disappointing fact triggers us to reconsider this hypothesis and to explore more effective treatment strategies.The drastic disturbance of glucose metabolism in the brain is one of the striking features of AD.A significant reduction in cerebral glucose consumption precedes overt clinical symptoms or brain atrophy, even for decades.Previous studies have demonstrated multiple defects in glucose and energy metabolism in AD patients.