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Ceruloplasmin functions as a ferroxidase in iron metabolism. Parkinson’s disease (PD) is characterized by an increase in brain iron. We postulated that lower circulating ceruloplasmin levels in PD would result in rapid brain iron accumulation and an earlier age of onset. Consecutive PD patients were separated into subgroups with younger (≤ 60 years, n = 62) and older ages of onset (> 60, n = 29), and compared to non-PD controls (n = 40). A oneway ANOVA comparing ceruloplasmin levels showed a very robust effect [ F(2,128) = 46.4, p < 1e-99]. Post hoc analysis demonstrated that the younger-onset PD subgroup [22.0 mg/dl ± 6.5 SD] had a lower mean ceruloplasmin level compared to the older-onset PD subgroup [35.7 ± 10.4] and controls [35.6 ± 8.4], whose levels did not differ from each other. Ceruloplasmin levels showed robust correlation with age of onset in all 91 PD patients [ r = 0.56, r2 = 0.31, p < 0.0001] but not in the non-PD controls [ r = 0.16, r2 = 0.03, not significant]. Mode of onset and duration of PD showed no relationship to ceruloplasmin. Serum copper and ferritin, available in most patients, did not differ between the PD subgroups. Younger-onset PD patients have significantly lower levels of serum ceruloplasmin compared to those with older-onset PD. Ceruloplasmin may play a role in the etiopathogenesis of younger-onset PD patients and merits further study. [ABSTRACT FROM AUTHOR]