Effect of coenzyme Q10 on the mitochondrial function of skin fibroblasts from Parkinson patients

Winkler-Stuck, Kirstin; Wiedemann, Falk R.; Wallesch, Claus‐W.; Kunz, Wolfram S.

doi:10.1016/j.jns.2004.02.003

Cited by 73 publications

(61 citation statements)

References 46 publications

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“…Skin fibroblast cultures of samples from 18 patients with PD were found to be deficient in respiratory chain complexes I and IV, indicating a generalized mitochondrial defect. 114 The respiratory chain defects might be secondary to an environmental toxin that is not brainselective and affects other tissues as well. Yet, several other studies on peripheral blood markers of oxidative stress, especially SOD activity, in PD reported contradictory results, [115][116][117] suggesting that the SN is more prone to oxidative stress than peripheral tissues.…”

Section: Miscellaneousmentioning

confidence: 99%

Lesions outside the CNS in Parkinson's disease

2009

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Parkinson's disease (PD) is not a simple movement disorder induced just by loss of dopaminergic neurons in the substantia nigra pars compacta. Apparently, the substantia nigra is not the only or the first brain region damaged in PD. Moreover, older and recent studies have shown that the degenerative process in PD is much more extensive and affects not only the central nervous system (CNS) but also the peripheral autonomic nervous system and the organs outside the brain that the latter innervates. These include mainly the gastrointestinal tract, the heart, kidneys, urogenital system, and skin. Additional extra-CNS organs that are involved in PD include the eye and the adrenal gland. This article reviews the anatomical, physiological, and clinical features of extracerebral manifestations of PD, and describes their relevance to the etiology and pathogenesis of the disease. It establishes this illness as a systemic CNS and peripheral disorder that warrants new hypotheses regarding its causation and progression.

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Section: Miscellaneousmentioning

confidence: 99%

Lesions outside the CNS in Parkinson's disease

2009

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“…60,61 Complex I and IV deficiencies in PD skin fibroblasts are improved by CoQ10. 62 Administration of CoQ10 has also inhibited NMDA-receptor-induced cell death to a greater degree in cultured medium spiny projection neurons of YAC46 mice, transgenic models of HD, relative to those of wild type mice. 63 Coenzyme Q10 has also been found to exert effects on α-synuclein and β-amyloid fibrils in vitro, possibly due to binding with hydrophobic and antioxidant motifs.…”

Section: 56mentioning

confidence: 93%

Coenzyme Q10 effects in neurodegenerative disease

Spindler

Beal²,

Henchcliffe³

2009

NDT

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“…CoQ10 is primarily found in its reduced form of ubiquinol, thereby having the ability to oxidise free radicals, and levels have been shown to be decreased in the aged cell (Bentinger et al 2007;Sohal and Forster 2007). The oral supplementation of CoQ10 has been used successfully in the treatment of hypertension, congenative heart failure and Parkinson's, all of which are associated with mitochondrial dysfunction (Langsjoen and Langsjoen 2008;Rosenfeldt et al 2003;Winkler-Stuck et al 2004). In addition oral supplementation of CoQ10 to rats decreases the incidence of mitochondrial complex I deletion often associated with aging and increases mitochondrial activity in the oocyte up to the level seen in young control mice (Bentov et al 2009;Ochoa et al 2011).…”

Section: Repair Of Mitochondrial Function: Quenching Rosmentioning

confidence: 99%