PGC-1α Expression Decreases in the Alzheimer Disease Brain as a Function of Dementia

Abstract
Alzheimer disease (AD) is a neurodegenerative disorder of the central nervous system. The neuropathological hallmarks of AD include extracellular amyloid-containing plaques and intracellular neurofibrillary tangles.1 The molecular events leading to the development of sporadic late-onset AD have not been defined. Advanced age is the largest AD risk factor and glucose/energy metabolism is decreased during aging.2-7 Recent evidence strongly supports the hypothesis that type 2 diabetes mellitus (T2D) is also a risk factor for AD.8-11 Moreover, recent evidence suggests that worsening in cerebral glucose metabolism is associated with progression of AD clinical dementia.12-16