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• W2023663306 abstract "To assess the potential of Drosophila to analyze clinically graded aspects of human disease, we developed a transgenic fly model to characterize Presenilin (PS) gene mutations that cause early-onset familial Alzheimer's disease (FAD). FAD exhibits a wide range in severity defined by ages of onset from 24 to 65 years [1Larner A.J. Doran M. Clinical phenotypic heterogeneity of Alzheimer's disease associated with mutations of the presenilin-1 gene.J. Neurol. 2006; 253: 139-158Crossref PubMed Scopus (186) Google Scholar]. PS FAD mutants have been analyzed in mammalian cell culture, but conflicting data emerged concerning correlations between age of onset and PS biochemical activity [2Duering M. Grimm M.O. Grimm H.S. Schröder J. Hartmann T. Mean age of onset in familial Alzheimer's disease is determined by amyloid beta 42.Neurobiol. Aging. 2005; 26: 785-788Abstract Full Text Full Text PDF PubMed Scopus (84) Google Scholar, 3Mehta N.D. Refolo L.M. Eckman C. Sanders S. Yager D. Perez-Tur J. Younkin S. Duff K. Hardy J. Hutton M. Increased Aβ42(43) from cell lines expressing presenilin 1 mutations.Ann. Neurol. 1998; 43: 256-258Crossref PubMed Scopus (90) Google Scholar, 4Murayama O. Tomita T. Nihonmatsu N. Murayama M. Sun X. Honda T. Iwatsubo T. Takashima A. Enhancement of amyloidß42 secretion by 28 different presenilin 1 mutations of familial Alzheimer's disease.Neurosci. Lett. 1999; 265: 61-63Crossref PubMed Scopus (106) Google Scholar]. Choosing from over 130 FAD mutations in Presenilin-1, we introduced 14 corresponding mutations at conserved residues in Drosophila Presenilin (Psn) and assessed their biological activity in transgenic flies by using genetic, molecular, and statistical methods. Psn FAD mutant activities were tightly linked to their age-of-onset values, providing evidence that disease severity in humans primarily reflects differences in PS mutant lesions rather than contributions from unlinked genetic or environmental modifiers. Our study establishes a precedent for using transgenic Drosophila to study clinical heterogeneity in human disease." @default.
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• W2023663306 date "2006-05-01" @default.
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• W2023663306 title "Modeling Clinically Heterogeneous Presenilin Mutations with Transgenic Drosophila" @default.
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• W2023663306 doi "https://doi.org/10.1016/j.cub.2006.04.004" @default.
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