title: Models of Alzheimer's disease: cellular and molecular aspects.
abstract: Glucose metabolism in the brain is an important process that influences many normal cellular processes, from neurotransmitter synthesis to ATP production. While cortisol and insulin have opposing effects on glucose metabolism, desensitization of the neuronal insulin receptor results in metabolic abnormalities. In the normal aging brain, glucose/energy metabolism is decreased slightly. In the majority of cases. Alzheimer's disease is sporadic and has a late onset. Therefore, age-related variations in cellular metabolism following the principle of self-organized criticality may come into focus with respect to the etiopathogenesis of this neurodegenerative disorder. As a possible primary abnormal event in late-onset sporadic DAT, a prolonged desensitization of the neuronal insulin receptor is assumed to be responsible for cascade-like abnormalities in oxidative energy metabolism and related metabolism with impacts on amyloid formation.
authors.affiliation: Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Federal Republic of Germany.
authors.forename: S
authors.initials: S
authors.lastname: Hoyer
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000375:Aging; D000544:Alzheimer Disease / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism*; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008959:Models, Neurological; D009474:Neurons / Q000378:metabolism; D011972:Receptor, Insulin / Q000502:physiology; D013312:Stress, Physiological
chemical_list: D000255:Adenosine Triphosphate; D011972:Receptor, Insulin; D005947:Glucose