Serum levels of coenzyme Q10 in patients with Parkinson's disease

Jiménez‐Jiménez, Félix Javier; Molina, J. A.; Bustos, F. de; García‐Redondo, Alberto; Gómez-Escalonilla, Carlos; Martínez-Salio, A; Berbel, A; Camacho, Ana; Zurdo, Martín; Barcenilla, Beatriz; Salamanca, Rafael Enrı́quez de; Arenas, Joaquı́n

doi:10.1007/s007020050015

Cited by 48 publications

(32 citation statements)

References 8 publications

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“…Jiménez-Jiménez et al [128] compared serum levels of CoQ 10 and the CoQ 10 /cholesterol ratio in 33 patients with PD and 31 matched controls. The mean serum CoQ 10 levels did not differ significantly between the two study groups.…”

Section: Serum Levels Of Coq 10 In Patients With Pdmentioning

confidence: 99%

Ubiquinone (Coenzyme Q<sub>10</sub>) and Mitochondria in Oxidative Stress of Parkinson’s Disease

et al. 2001

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Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease affecting approximately1% of the population older than 50 years. There is a worldwide increase in disease prevalence due to the increasing age of human populations. A definitive neuropathological diagnosis of Parkinson’s disease requires loss of dopaminergic neurons in the substantia nigra and related brain stem nuclei, and the presence of Lewy bodies in remaining nerve cells. The contribution of genetic factors to the pathogenesis of Parkinson’s disease is increasingly being recognized. A point mutation which is sufficient to cause a rare autosomal dominant form of the disorder has been recently identified in the α-synuclein gene on chromosome 4 in the much more common sporadic, or ‘idiopathic’ form of Parkinson’s disease, and a defect of complex I of the mitochondrial respiratory chain was confirmed at the biochemical level. Disease specificity of this defect has been demonstrated for the parkinsonian substantia nigra. These findings and the observation that the neurotoxin 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP), which causes a Parkinson-like syndrome in humans, acts via inhibition of complex I have triggered research interest in the mitochondrial genetics of Parkinson’s disease. Oxidative phosphorylation consists of five protein-lipid enzyme complexes located in the mitochondrial inner membrane that contain flavins (FMN, FAD), quinoid compounds (coenzyme Q₁₀, CoQ₁₀) and transition metal compounds (iron-sulfur clusters, hemes, protein-bound copper). These enzymes are designated complex I (NADH:ubiquinone oxidoreductase, EC 1.6. 5.3), complex II (succinate:ubiquinone oxidoreductase, EC 1.3.5.1), complex III (ubiquinol:ferrocytochrome c oxidoreductase, EC 1.10.2.2), complex IV (ferrocytochrome c:oxygen oxidoreductase or cytochrome c oxidase, EC 1.9.3.1), and complex V (ATP synthase, EC 3.6.1.34). A defect in mitochondrial oxidative phosphorylation, in terms of a reduction in the activity of NADH CoQ reductase (complex I) has been reported in the striatum of patients with Parkinson’s disease. The reduction in the activity of complex I is found in the substantia nigra, but not in other areas of the brain, such as globus pallidus or cerebral cortex. Therefore, the specificity of mitochondrial impairment may play a role in the degeneration of nigrostriatal dopaminergic neurons. This view is supported by the fact that MPTP generating 1-methyl-4-phenylpyridine (MPP⁺) destroys dopaminergic neurons in the substantia nigra. Although the serum levels of CoQ₁₀ is normal in patients with Parkinson’s disease, CoQ₁₀ is able to attenuate the MPTP-induced loss of striatal dopaminergic neurons.

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Section: Serum Levels Of Coq 10 In Patients With Pdmentioning

confidence: 99%

Ubiquinone (Coenzyme Q<sub>10</sub>) and Mitochondria in Oxidative Stress of Parkinson’s Disease

et al. 2001

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“…CoQ10 has membrane-stabilizing properties and also plays a vital role in ATP production [17]. Like the omega-3 fatty acid DHA, CoQ10 levels are decreased with aging [18], and in a number of neurodegenerative conditions [19]. …”

Section: Introductionmentioning

confidence: 99%

Effect of DHA and CoenzymeQ10 Against A�- and Zinc-Induced Mitochondrial Dysfunction in Human Neuronal Cells

Sadli¹,

Barrow²,

McGee

et al. 2013

Cell Physiol Biochem

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Background: Beta-amyloid (Aβ) protein is a key factor in the pathogenesis of Alzheimer's disease (AD) and it has been reported that mitochondria is involved in the biochemical pathway by which Aβ can lead to neuronal dysfunction. Coenzyme Q10 (CoQ10) is an essential cofactor involved in the mitochondrial electron transport chain and has been suggested as a potential therapeutic agent in AD. Zinc toxicity also affects cellular energy production by decreasing oxygen consumption rate (OCR) and ATP turnover in human neuronal cells, which can be restored by the neuroprotective effect of docosahexaenoic acid (DHA). Method: In the present study, using Seahorse XF-24 Metabolic Flux Analysis we investigated the effect of DHA and CoQ10 alone and in combination against Aβ- and zinc-mediated changes in the mitochondrial function of M17 neuroblastoma cell line. Results: Here, we observed that DHA is specifically neuroprotective against zinc-triggered mitochondrial dysfunction, but does not directly affect Aβ neurotoxicity. CoQ10 has shown to be protective against both Aβ- and zinc-induced alterations in mitochondrial function. Conclusion: Our results indicate that DHA and CoQ10 may be useful for the prevention, treatment and management of neurodegenerative diseases such as AD.

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“…113 Higher bilirubin levels were associated with worse motor symptoms at the time of PD diagnosis in a cohort of 75 de novo patients, but with better ones after 2-year follow-up, suggesting that higher bilirubin levels might depict a more pronounced neurodegenerative process, but are possibly related to improved outcomes over time. Higher UA levels were associated with slower motor progression and with a reduced risk of requiring levodopa treatment, in a secondary analysis of the DATATOP study.…”

Section: Oxidative Stressmentioning

confidence: 87%

Biomarkers of Parkinson's disease: recent insights, current challenges, and future prospects

Picillo¹,

Moccia²,

Spina³

et al. 2016

JPRLS

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Serum levels of coenzyme Q10 in patients with Parkinson's disease

Cited by 48 publications

References 8 publications

Ubiquinone (Coenzyme Q<sub>10</sub>) and Mitochondria in Oxidative Stress of Parkinson’s Disease

Ubiquinone (Coenzyme Q<sub>10</sub>) and Mitochondria in Oxidative Stress of Parkinson’s Disease

Effect of DHA and CoenzymeQ10 Against A�- and Zinc-Induced Mitochondrial Dysfunction in Human Neuronal Cells

Biomarkers of Parkinson's disease: recent insights, current challenges, and future prospects

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Serum levels of coenzyme Q10 in patients with Parkinson's disease

Cited by 48 publications

References 8 publications

Ubiquinone (Coenzyme Q<sub>10</sub>) and Mitochondria in Oxidative Stress of Parkinson’s Disease

Ubiquinone (Coenzyme Q<sub>10</sub>) and Mitochondria in Oxidative Stress of Parkinson’s Disease

Effect of DHA and CoenzymeQ10 Against A�- and Zinc-Induced Mitochondrial Dysfunction in Human Neuronal Cells

Biomarkers of Parkinson&#39;s disease: recent insights, current challenges, and future prospects

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Product

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Biomarkers of Parkinson's disease: recent insights, current challenges, and future prospects