Summary
Alzheimer’s diseases (AD) is a major health problem which will continue to intensify in magnitude as the elderly in the population continue to increase in number. The age at which AD strikes is variable, ranging from the fourth to tenth decades, with the greatest proportion of cases occurring in the seventh and eighth decades. A genetic component of this disorder has been strongly indicated by family and survey studies, as well as life table analyses (reviewed in St George-Hyslop et al. 1989). Genetic linkage and association studies of kindreds displaying evidence for familial AD (FAD) have led to the localization of gene defects responsible for this genetically heterogeneous disorder on chromosomes 14, 19 and 21. In a small set of FAD kindreds, mutations have been found in the amyloid beta protein precursor (APP) gene. Yet, the available data indicate that the identity of the genes responsible for the majority of late-onset (> 65 years) as well as early-onset inherited AD remain unknown. Powerful and novel advances in the methodology available for performing genetic linkage analyses on genetically complex disorders have made it feasible to scan the entire human genome in a relatively fast and easy manner for the purpose of localizing the genes responsible for, or predisposing to, inherited AD. Here we describe progress on attempts to further localize and identify various FAD gene defects throughout the genome, with special emphasis on the major early-onset gene defect residing on the long arm of chromosome 14.
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Tanzi, R.E. et al. (1994). The Diverse Molecular Nature of Inherited Alzheimer’s Disease. In: Masters, C.L., Beyreuther, K., Trillet, M., Christen, Y. (eds) Amyloid Protein Precursor in Development, Aging and Alzheimer’s Disease. Research and Perspectives in Alzheimer’s Disease. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-01135-5_17
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DOI: https://doi.org/10.1007/978-3-662-01135-5_17
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