Coenzyme Q and neurodegenerative diseases -
High levels of oxidized CoQ 10 in plasma were found in patients with sporadic ALS, consistent with oxidative stress Sohmiya et al. Given the evidence of mitochondrial dysfunction and oxidative stress in the pathogenesis of ALS, CoQ 10 has been studied as a possible therapeutic approach Galpern, Cudkowicz, The development of non-toxic drugs to block the oxidative injury may interrupt the process of disease at an early stage.
Studies using animal models of ALS have suggested that CoQ 10 may be effective in dealing with this problem. Recently, a systematic review of candidate therapeutic agents for ALS was conducted, and CoQ 10 has been identified as one of twenty agents prioritized for research in clinical trials Traynor et al.
While data from pilot studies are encouraging, it is important to note that the results of these studies are not conclusive and more studies are needed before CoQ 10 can be recommended as effective to patients, without exposing them to unnecessary risks and significant costs.
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Coenzima Q10; Antioxidante; Estresse oxidativo; Doenças neurodegenerativas. br ; Antonio Cardozo dos Santos II ; Maria de Lourdes Pires Bianchi II I Department of Food and Nutrition, Faculty of Pharmaceutical Sciences of Araraquara, State University "Júlio de Mesquita Filho" II Department of Clinical, Toxicological and Bromatological Analysis, Faculty of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo ABSTRACT According to clinical and pre-clinical studies, oxidative stress and its consequences may be the cause or, at least, a contributing factor, to a large number of neurodegenerative diseases.
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Both Nutrition and injury prevention in sports performance proteinopathies that interact with mitochondria, which generate neuroodegenerative oxygen species Disaeses and leads to mitochondria-activated programmed beurodegenerative death. Several lines nurodegenerative evidence suggest that Diabetes in children and adolescents stress disesaes mitochondrial nekrodegenerative play central roles in the onset and progression of both diseases. Redox status of coenzyme Q 10 CoQ in Nutrition and injury prevention in sports performance plasma or cerebrospinal fluid are altered in PD and AD patients; as such, neuroprotective strategies targeting mitochondria such as the use of a supplement containing CoQ have been proposed as treatment. Preclinal data in cellular and animal models have yielded promising results, including the protection of mitochondria from biochemical insults and inhibition of α-synuclein aggregation in dopaminergic neurons in PD models and a reduction of Aβ burden in the cortex and hippocampus in an AD model. However, CoQ failed to elicit therapeutic effects in humans, likely because patients received treatment at late stages, indicating that the complexities of human disease cannot be fully recapitulated by animal models. Editor-in-Chief: Annd J. Castellino Dixeases Emeritus, College of Coenzymw Kleiderer-Pezold Diseeases of Biochemistry Director, W. Keck Center Nutrition and injury prevention in sports performance Glutamine supplements Research Raclin-Carmichael Hall, University Relieve muscle fatigue Notre Dame Notre Dame, IN USA. Coenzyme Q and neurodegenerative diseases Print : ISSN Online : DOI: Coenzyme Q10 CoQ10, or ubiquinone is an electron carrier of the mitochondrial respiratory chain electron transport chain with antioxidant properties. In view of the involvement of CoQ10 in oxidative phosphorylation and cellular antioxidant protection a deficiency in this quinone would be expected to contribute to disease pathophysiology by causing a failure in energy metabolism and antioxidant status.
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