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Nondiscriminating Genes

Arch Neurol. 2000;57:28-29.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

EPIDEMIOLOGICAL AND molecular evidence suggests that there are multiple etiologies for Alzheimer disease (AD). Studies of the incidence and patterns of transmission in families demonstrate that relatives of affected individuals have an increased risk of developing AD compared with members of the general population.¹ With the exception of rare (probably <1%) cases harboring pathogenic mutations in the amyloid precursor protein or presenilin genes, susceptibility is governed by a complex interaction of genes and environmental factors. The most potent factor identified to date is the 4 allele of apolipoprotein E conferring a relative risk of between 2.7 and 3.2 in persons having a single copy and between 12.5 and 14.9 in those homozygous for this factor.² Notably, these conclusions were drawn from studies of largely white populations.

The African American population of persons older than 65 years is growing even faster than the white population in this age group, meaning that . . . [Full Text of this Article]

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