ABSTRACT
The major and quantitatively only significant pathways for cerebral oxidative metabolism are glycolysis, pyruvate dehydrogenase, the Krebs tricarboxylic acid cycle, and electron transport. In Alzheimer’s disease (AD), decreases in cerebral metabolism occur even in incipient AD, before major clinical changes are evident. Although a minority of unusually healthy elderly people can be identified in whom cerebral oxidative metabolism is indistinguishable from the young adult population, cerebral metabolism declines with age in the elderly population as a whole and particularly in the large fraction of the population who have cardiovascular risk factors. Reductions in cerebral metabolic rate in AD are incontrovertable. It has been suggested that the characteristic reduction in cerebral metabolism in AD is due to a decrease in cerebral activity accompanying the dementia. The neuropsychologic deficits which accompany impaired cerebral oxidative metabolism have been exhaustively described, notably in the aviation literature of the 1930s to the 1950s in regard to pure hypoxia.
