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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

Revue neurologique

Publication Date

01/1999

Volume

155 Suppl 4

Pages

S10 - S16

Addresses

Department of Epidemiology & Biostatistics, Erasmus University Medical School, Rotterdam, The Netherlands.

Keywords

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