Age as Risk Factor for Sporadic Dementia of the Alzheimer Type?

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Abstract
Normal brain aging is accompanied by a slight but persistent reduction in energy formation and an increase in energy demand. Stress conditions aggravate energy shortage particularly in old age. Mitochondrial dysfunction in both ATP formation and ATP release may be assumed to be causative for the reduced availability of energy in cerebral cells leading to diminished cellular work. In this respect, aging may be considered as a contributing risk factor for sporadic late-onset dementia of the Alzheimer type. Metabolically, this disorder seems to be characterized also by an early energy shortage in cerebral cells with the same consequences for the disturbance of cellular work. However, the causative abnormality may be seen in a perturbation of the control of cerebral glucose metabolisms, in all probability mediated by a desensitization of the neuronal insulin receptor.