Is sporadic Alzheimer disease the brain type of non-insulin dependent diabetes mellitus? A challenging hypothesis.
The hypothesis is forwarded that sporadic late-onset Alzheimer disease is caused by non-insulin dependent diabetes mellitus which is confined to the brain. This hypothesis is based on the findings of Frölich and coworkers (this volume) who clearly demonstrate a perturbation of the neuronal insulin/ insulin receptor signal transduction pathway which is considered to be the pathobiochemical basis for the drastic reduction in glucose/energy metabolism in Alzheimer brain. As a consequence of this abnormality, advanced glycation end products are formed. Münch et al. (this volume) evaluate the impacts of the latter related to oxidative stress and the formation of beta-amyloid and neurofibrillary tangles.
Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Federal Republic of Germany.
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D017668:Age of Onset; D000544:Alzheimer Disease / Q000209:etiology / Q000503:physiopathology*; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000503:physiopathology*; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism; D017127:Glycation End Products, Advanced; D006801:Humans; D007328:Insulin / Q000502:physiology; D008959:Models, Neurological; D009474:Neurons / Q000502:physiology*; D011972:Receptor, Insulin / Q000502:physiology; D015398:Signal Transduction
D017127:Glycation End Products, Advanced; D007328:Insulin; D011972:Receptor, Insulin; D005947:Glucose