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In recent years, considerable progress has been made in unraveling the etiology of Alzheimer's disease (AD). Dominant mutations have been identified, in the beta-amyloid precursor protein gene (APP), and in two homologous genes presenilin 1 (PSEN-1) and presenilin 2 (PSEN-2). The contribution of these mutations to the occurrence of AD in the general population is estimated to be lower than 1p. 100. A genetic risk factor of more importance on the population level is the Apolipoprotein E (APOE) gene that may explain up to 17p. 100 of the prevalence of AD in the general population. It is clear that other yet unknown genes must be involved in the etiology of AD. Two loci on chromosome 12 have been suggested, but no consistent effect could be found. Important progress with regard to non-genetic risk factors concerns the role of vascular and endocrine factors in the pathogenesis. Of major interest for the prevention of AD will be the interaction of genetic and non-genetic risk factors. Large scale, long term follow-up studies, ongoing at present, may clarify this issue.

Type

Journal article

Journal

Rev Neurol (Paris)

Publication Date

1999

Volume

155 Suppl 4

Pages

S10 - S16

Keywords

Aged, Alzheimer Disease, Amyloid beta-Protein Precursor, Apolipoproteins E, Chromosome Aberrations, Chromosome Disorders, Environment, Exons, Gene Expression, Genotype, Humans, Point Mutation, Polymorphism, Genetic, Risk Factors