Geriatrics

Alzheimer's disease and related disorders annual, 2002 by Jeffrey L Cummings, Serge Gauthier PDF

By Jeffrey L Cummings, Serge Gauthier

ISBN-10: 1841842346

ISBN-13: 9781841842349

Given the advance of recent healing techniques and items, Serge Gauthier and Jeffrey Cummings have compiled an inventory of up to date themes with a purpose to be of curiosity essentially to neurologists targeting Alzheimer's illness, and in addition to psychiatrists and geriatricians. The individuals, all revered of their subspecialties, have written up to date, comprehensively referenced chapters which should offer suggestions in addition to stimulate dialogue on the place present remedy is heading.

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23. Lassmann H, Bancher C, Breitschopf H et al. Cell death in Alzheimer’s disease evaluated by DNA fragmentation in situ. Acta Neuropathol 1995; 89:35–41. 24. Desjardins P, Ledoux S. Expression of ced-3 and ced-9 homologs in Alzheimer’s disease cerebral cortex. Neurosci Lett 1998; 244:69–72. 25. Kitamura Y, Shimohama S, Kamoshima W et al. Alteration of proteins regulating apoptosis, Bcl2, Bcl-x, Bax, Bak, Bad, ICH-1 and CPP32, in Alzheimer’s disease. Brain Res 1998; 780:260–269. 26. Selznick LA, Holtzman DM, Han BH et al.

Evidence for neuronal plasticity? Neurosci Lett 1987; 76:228–232. 79. Cotman CW, Anderson KJ. Synaptic plasticity and functional stabilization in the hippocampal formation: possible role in Alzheimer’s disease. Adv Neurol 1988; 47:313–335. 80. Jorgensen OS, Brooksbank BW, Balazs R. Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease. J Neurol Sci 1990; 98:63–79. 81. Mirmiran M, van Someren EJ, Swaab DF. Is brain plasticity preserved during aging and in Alzheimer’s disease?

At this point, it was expected that overexpression of APP would reveal whether the generation of supranormal levels of Aβ peptide would invariably lead to the known pathology of AD. Even more importantly, it was thought that with the study of transgenic mice of various ages, the relative contribution of Aβ deposition to the disease process could be ascertained: Aβ was either an important initiator of the well-described pathological cascade or was merely an inert deposit, a by-product of dying neurons.

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Alzheimer's disease and related disorders annual, 2002 by Jeffrey L Cummings, Serge Gauthier


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