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Altered systemic iron metabolism in Parkinson's disease

From the Gertrude H. Sergievsky Center (Drs. Logroscino, Marder, Cote, and Mayeux); the Departments of Neurology (Drs. Logroscino, Marder, Cote, and Mayeux), Psychiatry (Dr. Mayeux), and Pharmacology (Dr. Graziano), College of Physicians and Surgeons; Divisions of Epidemiology (Dr. Mayeux) and Environmental Health Sciences (Drs. Graziano and Freyer, and V. Slavkovich and N. LoIacono), School of Public Health, Columbia University, New York, NY; and Divisione di Neurologia (Dr. Logroscino), Ospedale Miulli Acquaviva (Bari), Italy.

Address correspondence and reprint requests to Dr. Richard Mayeux, G.H. Sergievsky Center, 630 West 168th Street, New York, NY 10032.

Iron deposition in the substantia nigra in Parkinson's disease has been 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 death. Remarkably, there are few data available concerning systemic iron metabolism in Parkinson's disease. We measured total iron binding capacity and circulating iron, ferritin, transferrin, and transferrin receptors; calculated transferrin saturation; and estimated dietary iron intake in patients with idiopathic Parkinson's disease and in controls. Concentrations of circulating iron, ferritin, and transferrin as well as total iron binding capacity and transferrin saturation were significantly lower in patients than controls. There were no differences in transferrin receptors or dietary intake of iron. The decrease in levels of systemic ferritin and transferrin and the total iron binding capacity 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 defect in the systems that regulate the synthesis of the major proteins of iron metabolism in the liver as well as the brain in Parkinson's disease that may, over time, expedite entry of iron into the brain and decrease iron in the extracellular compartment.

Supported by federal grants NS32527 (R.M.), AG07232 (R.M.), and ES06831(J.G.), from the National Institute of Health, and by grants from the Parkinson's Disease Foundation and the John and Evelyn Kossak Foundations, Inc.

Received January 23, 1997. Accepted in final form May 8, 1997.

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