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Mitochondrial therapy for Parkinson’s disease: Neuroprotective pharmaconutrition may be disease-modifying

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Authors: Richard Kones

Published Date September 2010 Volume 2010:2 Pages 185 - 198
DOI: http://dx.doi.org/10.2147/CPAA.S12082

Richard Kones
Cardiometabolic Research Institute, Houston, TX, USA

Abstract: Progressive destruction of neurons that produce dopamine in the basal ganglia of the brain, particularly the substantia nigra, is a hallmark of Parkinson’s disease. The syndrome of the Parkinsonian phenotype is caused by many etiologies, involving multiple contributing mechanisms. Characteristic findings are pathologic inclusions called Lewy bodies, which are protein aggregates inside nerve cells. Environmental insults are linked with the disease, and a number of associated genes have also been identified. Neuroinflammation, microglia activation, oxidative stress, and mitochondrial dysfunction are central processes producing nerve damage. In addition, protein misfolding, driven by accumulation and condensation of a-synuclein, compounded by inadequate elimination of defective protein through the ubiquitin-proteasome system, promote apoptosis. Current pharmacologic therapy is palliative rather than disease-modifying, and typically becomes unsatisfactory over time. Coenzyme Q10 and creatine, two agents involved in energy production, may be disease-modifying, and able to produce sufficient beneficial pathophysiologic changes in preclinical studies to warrant large studies now in progress. Use of long-chain omega-3 fatty acids and vitamin D in PD are also topics of current interest.
Keywords: Parkinson’s disease, mitochondria, inflammation, reactive oxygen species, apoptosis, ubiquinone, creatine, polyunsaturated omega-3 fatty acids, vitamin D




 

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