It was suggested that in contrast to the E4 allele, the E2 allele of the apolipoprotein E gene (APOE*2) has a protective effect for late-onset Alzheimer's disease and early-onset Alzheimer's disease (EOAD). We studied the role of the APOE*2 allele in the pathogenesis of EOAD in a Dutch population-based study of 175 probable EOAD patients with onset age at or before 65 years and 532 age-matched controls. In our population, there was no evidence for a protective effect of the APOE*2 allele on the risk of EOAD. However, our data show that among EOAD patients, survival for APOE*2 carriers was significantly reduced. When restricting the analysis to patients ascertained early after diagnosis at a stage of disease when mortality is low, our data suggest an increased risk of EOAD for subjects with APOE2E2, APOE2E3, APOE3E4, and APOE4E4 genotypes.

, , , , , , , , , , , , , , , , , ,
Annals of Neurology
Erasmus MC: University Medical Center Rotterdam

van Duijn, C., de Knijff, P., Wehnert, A., de Voecht, J., Bronzova, J., Havekes, L. M., … Hofman, A. (1995). The apolipoprotein E ε 2 allele is associated with an increased risk of early-onset Alzheimer's disease and a reduced survival. Annals of Neurology, 37, 605–610. Retrieved from