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From the Departments of Epidemiology & Biostatistics (Drs. Harhangi, van Duijn, Hofman, and Breteler) and Neurology (Dr. de Rijk), Erasmus Medical Center Rotterdam, The Netherlands; and the Flanders Interuniversity Institute for Biotechnology (Dr. Van Broeckhoven), Born-Bunge Foundation, University of Antwerp, Belgium.
Address correspondence and reprint requests to Dr. Breteler, Department of Epidemiology & Biostatistics, Erasmus Medical Center Rotterdam, P.O.Box 1738, 3000 DR, Rotterdam, The Netherlands; e-mail: breteler{at}epib.fgg.eur.nl
OBJECTIVE: To study the association between APOE genotype and PD with or without dementia.
METHODS: The study formed part of the Rotterdam Study, a prospective, population-based cohort study on the frequency, etiology, and prognosis of chronic diseases. The cohort examined for PD consisted of 6969 independently living or institutionalized inhabitants from a suburb of Rotterdam, the Netherlands, aged 55 years or older. All participants were screened at baseline (1990 to 1993) and at follow-up (1993 to 1994) for symptoms of parkinsonism by study physicians; screen positives received a diagnostic workup by a neurologist.
RESULTS: APOE genotyping was available for 107 PD patients (26 with and 81 without dementia) and 4805 non-PD control subjects. The presence of at least one 
2 allele significantly increased the risk of PD (OR = 1.7; 95% CI, 1.0 to 2.8). When we looked separately for demented and nondemented PD patients as compared with nonparkinsonian controls, APOE did not appear to be associated with PD without dementia, but both the 2 and the 4 allele increased the risk of PD with dementia (OR = 5.6; 95% CI, 2.0 to 15.2 and OR = 3.6; 95% CI, 1.3 to 9.9). The risk of dementia for 4 allele carriers was not significantly different for persons with or without PD. However, the 2 allele strongly increased the risk of dementia in patients with PD (interaction p < 0.007).
CONCLUSIONS: In the elderly the APOE-2 allele increases the risk of PD and, in particular, the risk of PD with dementia.
Key words: APOE—Parkinson’s disease—Dementia—Genetics—Epidemiology.
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