By N M Hooper; Humana Press
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73) demonstrated that caspase-mediated processing of PS-1 and PS-2 is not required for Αβ42 production or the effect of mutant PS proteins on abnormal Αβ generation. The Genetics of Alzheimer’s Disease 33 All PS-1 and PS-2 mutations analyzed have demonstrable effects on the generation of the more toxic Αβ42 fragment. Αβ production in fibroblasts and plasma levels of Αβ in carriers of PS mutations indicate altered APP processing in favor of Αβ 42 generation (74,75). Similar increases in Αβ42 production results were obtained in transgenic mice overexpressing PS mutations (76).
Mutations in the presenilins may also render cells more vulnerable to apoptotic cell death, or neuronal death in AD may result from altered interaction of the presenilins with other proteins such as the catenins (79). 7. Association Studies in Alzheimer’s Disease Association studies typically compare a marker frequency in patients with that in control subjects. The studies implicate either the gene from which the polymorphic marker was derived or a nearby susceptibility gene in linkage disequilibrium with the marker.
90. Kang, D. , Hansen, L. , et al. (1997) Genetic association of the low density lipoprotein receptor-related protein gene (LRP), an apolipoprotein E receptor with late onset Alzheimer’s disease. Neurology 49, 56–61. 91. , Gauntlett, A. , Mullan, M. (1997) No association between the low density lipoprotein receptor related protein and late onset Alzheimer’s disease. Am. J. Hum. Genet. 61, 1143. 92. , Han, S. , Clark, R. , et al. (1996) Genetic association between intronic polymorphism in presenilin-1 gene and late-onset Alzheimer’s disease.