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Mutations at three genetic loci associated with early-onset AD have been identified. The first identified AD gene was the amyloid precursor protein (APP) gene located on chromosome 21 (Goate et al. 1991). Since this first report of a missense mutation (i.e., one amino acid is substituted for another) associated with AD on this gene, over 20 different missense mutations in APP that can cause AD have been identified (Alzheimer Disease and Frontotemporal Dementia Mutation Database 2008). Individuals with one of these APP mutations generally have onset of disease between ages 40 and 60 years, though occasionally later ages of onset can occur (Theuns et al. 2006). More recently, families with duplications of APP, leaving the mutation carrier with a total of three copies of the gene on their two chromosomes, have been reported (Rovelet-Lecrux et al. 2006; Sleegers et al. 2006). These families had early-onset AD associated with cerebral amyloid angiopathy and intracerebral hemorrhage. Although the identification of mutations in APP has been key to advancing our understanding of the genetic causes of AD, all APP mutations reported to date account for the disease in fewer than 100 families worldwide (Alzheimer Disease and Frontotemporal Dementia Mutation Database 2008).

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