Risk of dementia among relatives of Alzheimer's disease patients in the MIRAGE study

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Abstract
Family, epidemiologic, and molecular studies have implicated genetic factors in the etiology of AD. [7] Some familial cases with age at onset in the fourth and fifth decades have defects in genes recently identified on chromosomes 1 and 14. [8,9] The frequency of these mutations in the population is not yet known. Manifestation of early-onset AD is also associated with mutations in the beta-amyloid precursor protein (APP) gene on chromosome 21, but this is a very rare cause of AD. [10-13] A genomic search localized a gene for familial late-onset AD to chromosome 19, [14] and association studies of loci in this region subsequently implicated the apolipoprotein E (ApoE) gene as a likely susceptibility locus. [15] The element 4 allele of ApoE is several times more frequent in sporadic patients with late-onset disease than in cognitively normal persons in the general population. [16] This finding has been replicated in numerous clinic-based and cross-sectional patient populations including those enriched for early-onset disease [17-22] (for a review see reference 23).

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