Neurodegeneration, Alzheimer's disease, and beta-amyloid toxicity.

In its majority, Alzheimer's disease is sporadic and with late onset. Therefore, age-related disturbances in cellular metabolism may come into focus with respect to the etiopathogenesis of this neurodegenerative disorder. As a possible primary abnormal event in sporadic Alzheimer's disease, a desensitization of the neuronal insulin receptor and the subsequent deficits in ATP and acetylcholine are discussed with its impact on protein processing in general and beta-amyloid formation in particular, and neurotoxicity of the latter.