Prevention of progression in Parkinson's disease.

Jan Aaseth, Petr Dusek, Per M Roos

Journal: Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine 2019;31(5):737-747

PMID: 30030679

Abstract

Environmental influences affecting genetically susceptible individuals seem to contribute significantly to the development of Parkinson's disease (PD). Xenobiotic exposure including transitional metal deposition into vulnerable CNS regions appears to interact with PD genes. Such exposure together with mitochondrial dysfunction evokes a destructive cascade of biochemical events, including oxidative stress and degeneration of the sensitive dopamine (DA) production system in the basal ganglia. Recent research indicates that the substantia nigra degeneration can be decelerated by treatment with iron binding compounds such as deferiprone. Interestingly compounds known to decrease PD risk including caffeine, niacin, nicotine and salbutamol also possess iron binding properties. Adequate function of antioxidative mechanisms in the vulnerable brain cells can be restored by acetylcysteine supplementation to normalize intracellular glutathione activity. Other preventive measures to reduce deterioration of dopaminergic neurons may involve life-style changes such as intake of natural antioxidants and physical exercise. Further research is recommended to identify therapeutic targets of the proposed interventions, in particular protection of the DA biosynthesis by oxygen radical scavengers and iron binding agents.

Address: Research Department, Innlandet Hospital Trust, Brumunddal, Norway.; Inland Norway University of Applied Sciences, Elverum, Norway.; Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University, Praha 2, Czech Republic.; General University Hospital in Prague, Prague, Czech Republic.; Department of Radiology, First Faculty of Medicine, Charles University, Praha 2, Czech Republic.; Institute of Environmental Medicine, Karolinska Institutet, Solna, Sweden. [email protected].; Department of Clinical Physiology, Capio St. Görans Hospital, Stockholm, Sweden. [email protected].
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