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.
Hoyer
S
S
Department of Pathochemistry and General Neurochemistry, University of Heidelberg, FRG.
D000544:Alzheimer Disease / Q000503:physiopathology*; D016229:Amyloid beta-Peptides / Q000096:biosynthesis / Q000502:physiology*; D000818:Animals; D006801:Humans; D009410:Nerve Degeneration / Q000502:physiology*
D016229:Amyloid beta-Peptides