By N M Hooper; Humana Press
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Additional resources for Alzheimer's disease : methods and protocols
And Owen, M. J. (1996) Presenilin polymorphism and Alzheimer’s disease. Lancet 347, 1185. 94. , Lambert, J. , et al. (1996) Presenilin polymorphism and Alzheimer’s disease. Lancet 347, 1560–1561. 95. Scott, W. , Growdon, J. , Roses, A. , Haines, J. , Pericak-Vance, M. A. (1996) Presenilin polymorphism and Alzheimer’s disease. Lancet 347, 1186–1187. 96. Scott, W. , Yamaoka, L. , Locke, P. , Rosi, B. , Gaskell, P. , Saunders, A. , et al. (1997) No association or linkage between an intronic polymorphism of presenilin-1 and sporadic or late onset familial Alzheimer’s disease.
89. , Lambert, J. , et al. (1997) Association between the low density lipoprotein receptor-related protein (LRP) and Alzheimer’s disease. Neurosci. Lett. 227, 68–70. 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.
Elegans causes an egg-laying defective (Egl) phenotype. Normal human presenilins can substitute for the C. elegans sel-12 and rescue the Egl phenotype (67). Mutant presenilins were found to incompletely rescue the sel-12 mutant phenotype suggesting they have lower presenilin activity. PS-1 homology to spe-4 in C. elegans, a protein involved in sperm morphogenesis, suggests a role in protein transport and storage. PS-1 knockout mice die during early embryogenesis due to defects in somite segmentation.