Abstract
Recent progress in understanding the molecular basis of Alzheimer’s disease (AD) can be attributed mainly to linkage analysis and positional cloning of gene mutations associated with familial AD (FAD) pedigrees. The majority of early-onset AD cases are familial, and co-segregate with mutations in three known genes: these are the amyloid precursor protein (APP) gene on chromosome 21; the presenilin-1 (PS-1) gene located on chromosome 14; and the presenilin homologue, PS-2, on chromosome 1. Mutations in APP, PS-1 and PS-2, are inherited as autosomal dominant traits with complete or a very high degree of penetrance. A significant proportion of early onset AD cannot be attributed to mutations in any one of these genes, however, and so it is clear that other loci remain to be identified.
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Shearman, M.S. (1998). Amyloid-β Hypothesis of Alzheimer’s Disease. In: Fisher, A., Hanin, I., Yoshida, M. (eds) Progress in Alzheimer’s and Parkinson’s Diseases. Advances in Behavioral Biology, vol 49. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5337-3_27
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DOI: https://doi.org/10.1007/978-1-4615-5337-3_27
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