ALTERED SYSTEMIC IRON-METABOLISM IN PARKINSONS-DISEASE

Iron deposition in the substantia nigra in Parkinson's disease has bee n associated with an increase in lactoferrin receptors and a reduction in ferritin concentration. This accumulation of iron in the brain may accelerate free radical formation, lipid peroxidation, and neuronal d eath. Remarkably, there are few data available concerning systemic iro n metabolism in Parkinson's disease. We measured total iron binding ca pacity and circulating iron, ferritin, transferrin, and transferrin re ceptors; calculated transferrin saturation; and estimated dietary iron intake in patients with idiopathic Parkinson's disease and in control s. Concentrations of circulating iron, ferritin, and transferrin as we ll as total iron binding capacity and transferrin saturation were sign ificantly lower in patients than controls. There were no differences i n transferrin receptors or dietary intake of iron. The decrease in lev els of systemic ferritin and transferrin and the total iron binding ca pacity parallels observations in a Parkinson's disease brain, but the reductions in serum iron concentrations and transferrin saturation do not, and were unexpected. These results suggest the existence of a def ect in the systems that regulate the synthesis of the major proteins o f iron metabolism in the liver as well as the brain in Parkinson's dis ease that may, over time, expedite entry of iron into the brain and de crease iron in the extracellular compartment.