Cell and Animal Models in Aging and Dementia Research by H. Oberpichler-Schwenk (auth.), Prof. Dr. S. Hoyer, Dr. D.

By H. Oberpichler-Schwenk (auth.), Prof. Dr. S. Hoyer, Dr. D. Müller, Dr. K. Plaschke (eds.)

Although age has been famous as a chance issue for late-onset dementia of Alzheimer sort, its etiology is unknown as but. a number of age-related metabolic abnormalities may well hence develop into very important for the pathogenesis of the late-onset shape. reports on the cellular/molecular point in mind tissue are attainable publish mortem, yet lack details at the starting of the illness. during this complement, assorted techniques are handled tips on how to result in structural and/or metabolic abnormalities in proper telephone cultures, in mind slices and in experimental animals, and the way behavioral alterations parallel the metabolic variations.

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Within 4-12 hours after the onset of glucose-deprivation the [Ca2 +]j begins to rise, during which time the neurons appear to be undamaged. However, by 12-16 hours there is a marked increase in [Ca2 +]j and the neurons die rapidly within the next 4 hours (Cheng and Mattson, 1991). We found that neurons deprived of glucose exhibited similar antigenic changes in tau and ubiquitin as seen in glutamate toxicity and the NFT of AD (Cheng and Mattson, 1992b). e. , 1989; Cheng and Mattson, 1991, 1992a).

Raven Press, New York, p 81 Hoyer S (1988) Glucose and related brain metabolism in dementia of Alzheimer type and its morphological significance. Age 11: 158-166 42 V. L. Smith-Swintosky and M. P. Mattson Hoyer S, Oesterreich K, Wagner 0 (1988) Glucose metabolism as the site of the primary abnormality in early-onset dementia of Alzheimer type? 1 Neurol 235: 143-148 Iwamoto N, Thangnipon W, Crawford C, Emson PC (1991) Localization of calpain immunoreactivity in the senile plaques and in neurones undergoing neurofibrillary degeneration in Alzheimer's disease.

L. Smith-Swintosky and M. P. , NEUROTROPHINS bFGF IGF's SECRETORY CLEAVAGE ~ APP R CEP OR + ~ ! ±1 ~ ~ + .. [Ca li ++ FREE RADICALS r +1 2 ~ CALCIUM BINDING PROTEIN Ca2+-DEPENDENT PROTEASES CYTOSKELETAl MEMBRANE DAMAGE CELL DEATH Fig. 2. Possible mechanisms contributing to perturbated calcium and free radical metabolism in AD. Schematic diagram of the proposed interactions between ~APP, glutamate, growth factors and intracellular calcium with respect to cell degeneration and subsequent death. Amyloid precursor protein (PAPP) can be cleaved within the A~ region by an a-secretase to generate secreted forms of APP.

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