Telomeres constitute the protective ends of chromosomes. They become shorter after each cell division, and therefore, telomere length is considered as an indicator of cellular aging. Interestingly, both inflammation and oxidative stress, which play a role in the etiology of Parkinson's disease (PD), may accelerate telomere shortening. Furthermore, it has been suggested that leukocyte telomere shortening may be accelerated in PD. To replicate the earlier findings, we analyzed telomere length of peripheral blood leukocytes in a sample of 131 PD patients (aged 66.8 ± 9.7 years) and 115 controls (aged 65.4 ± 9.8 years) from Finland. As expected, age associated significantly with telomere length (p = .01). However, telomere length did not differ significantly between PD patients and controls (p = .54). Furthermore, extremely short telomeres were not more frequent in PD patients than in controls, as suggested in an earlier study. Our results do not support the concept of accelerated leukocyte telomere shortening in PD.