By Jeffrey L Cummings, Serge Gauthier

Given the advance of recent healing recommendations and items, Serge Gauthier and Jeffrey Cummings have compiled a listing of latest subject matters that allows you to be of curiosity basically to neurologists targeting Alzheimer's illness, and in addition to psychiatrists and geriatricians. The members, all revered of their subspecialties, have written updated, comprehensively referenced chapters which should supply assistance in addition to stimulate dialogue on the place present therapy is heading.

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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. In situ immunodetection of neuronal caspase-3 activation in Alzheimer disease. J Neuropathol Exp Neurol 1999; 58:1020–1026. 27.

Neurology 1995; 45: 51–55. 108. Breitner JC, Gau BA, Welsh KA et al. Inverse association of antiinflammatory treatments and Alzheimer’s disease: initial results of a co-twin control study. Neurology 1994; 44:227–232. 3 Transgenic models of Alzheimer’s disease Josephine Nalbantoglu Before the elucidation of the genetic mutations involved in familial Alzheimer’s disease (AD), most of the studies of AD were based on the pathological characteristics of brain tissue obtained at autopsy from patients that had been diagnosed clinically as suffering from dementia.

An analysis of apoptosis-related molecules in the caspase-2 null mice revealed that they had a compensatory increase of about fourfold in caspase-9 and an almost threefold increase in the protein DIABLO/Smac, which acts to inhibits the IAPs. In cells lacking caspase-2, trophic factor deprivation induced death depends on caspase 9 and caspase 3 and the cells can be rescued by antisense inhibition of either of these molecules. 48 A similar ‘backup’ pathway exists in caspase-2 null cells exposed to Aβ (Troy et al, in preparation).

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