Correction to: Orally delivered water soluble coenzyme Q10 (Ubisol-Q10) blocks on-going neurodegeneration in rats exposed to paraquat: potential for therapeutic application in Parkinson’s disease

Introduction. Coenzyme Q10, also known as Ubiquinone, is a substance now being used as a dietary supplement in many countries including the Philippines. It has also been the focus of several researches as treatment for several diseases including Parkinson’s Disease. Several studies have shown that Coenzyme Q10 inhibits mitochondrial dysfunction in Parkinson’s Disease, hence delaying its progression. Objectives. The objective of this study is to assess and summarize the available evidence on the efficacy and safety of Coenzyme Q10 administration in the prevention of the progression of early Parkinson’s Disease. Methods. This is meta-analysis of randomized controlled trials on the use of Coenzyme Q10 in Parkinson’s Disease. A literature search in several databases was conducted for relevant studies. Three randomized controlled trials met the inclusion criteria. The efficacy of Coenzyme Q10 were measured using the total and the component scores of the Unified Parkinson Disease Rating Scale on follow-up. On the other hand, safety were measured using the withdrawal rate and the associated adverse reactions during the therapy of CoQ10. The Review Manager Software was utilized for the meta-analysis. Results. Compared to Placebo, treatment of CoQ10 did not show any significant difference in the mean scores of the UPDRS mental and ADL scores. Interestingly, the UPDRS motor score showed a significant difference between Coenzyme Q10 and placebo, but no significant difference when a subgroup analysis between high-dose (-4.03 [-15.07-7.01], p-value 0.47, I2 67%, P for heterogeneity 0.08) and low-dose Coenzyme Q10 (0.53 [-0.891.94], p-value 0.47, I2 34%, P for heterogeneity 0.22) was done. Overall, there was no significant difference in the total UPDRS score (0.68 [-0.61-1.97], p-value 0.30, I2 0%, P for heterogeneity 0.70). The most common side effects of the use of Coenzyme Q10 are anxiety, back pain, headache, sore throat, nausea, dizziness and constipation. Conclusion. Contrary to some animal and human studies, this meta-analysis showed that the use of CoQ10 results to nonsignificant improvement in all components of the UPDRS scores as opposed to placebo. However, the use of CoQ10 is tolerated and seems to be safe but further studies are needed to validate this finding.

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Roles of Wnt/β-Catenin Signaling in Controlling the Dopaminergic Neuronal Cell Commitment of Midbrain and Therapeutic Application for Parkinson’s Disease

Trends in Cell Signaling Pathways in Neuronal Fate Decision ◽

10.5772/53282 ◽

2013 ◽

Cited By ~ 1

Author(s):

Liang-Wei Chen

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Neuronal Cell ◽

Therapeutic Application ◽

Dopaminergic Neuronal Cell ◽

Cell Commitment

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Neuroprotective Actions of Coenzyme Q10 in Parkinson's Disease

Methods in Enzymology - Quinones and Quinone Enzymes, Part B ◽

10.1016/s0076-6879(04)82027-5 ◽

2004 ◽

pp. 488-509 ◽

Cited By ~ 34

Author(s):

S Sharma ◽

M Kheradpezhou ◽

S Shavali ◽

H.El Refaey ◽

J Eken ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Coenzyme Q10 ◽

Neuroprotective Actions

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The Role of Oxidative Stress in Parkinson’s Disease

Antioxidants ◽

10.3390/antiox9070597 ◽

2020 ◽

Vol 9 (7) ◽

pp. 597 ◽

Cited By ~ 4

Author(s):

Kuo-Hsuan Chang ◽

Chiung-Mei Chen

Keyword(s):

Oxidative Stress ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Vitamin E ◽

Coenzyme Q10 ◽

Conclusive Evidence ◽

Abnormal Accumulation ◽

Progressive Neurodegeneration ◽

Antioxidative Treatment

Parkinson’s disease (PD) is caused by progressive neurodegeneration of dopaminergic (DAergic) neurons with abnormal accumulation of α-synuclein in substantia nigra (SN). Studies have suggested the potential involvement of dopamine, iron, calcium, mitochondria and neuroinflammation in contributing to overwhelmed oxidative stress and neurodegeneration in PD. Function studies on PD-causative mutations of SNCA, PRKN, PINK1, DJ-1, LRRK2, FBXO7 and ATP13A2 further indicate the role of oxidative stress in the pathogenesis of PD. Therefore, it is reasonable that molecules involved in oxidative stress, such as DJ-1, coenzyme Q10, uric acid, 8-hydroxy-2’-deoxyguanosin, homocysteine, retinoic acid/carotenes, vitamin E, glutathione peroxidase, superoxide dismutase, xanthine oxidase and products of lipid peroxidation, could be candidate biomarkers for PD. Applications of antioxidants to modulate oxidative stress could be a strategy in treating PD. Although a number of antioxidants, such as creatine, vitamin E, coenzyme Q10, pioglitazone, melatonin and desferrioxamine, have been tested in clinical trials, none of them have demonstrated conclusive evidence to ameliorate the neurodegeneration in PD patients. Difficulties in clinical studies may be caused by the long-standing progression of neurodegeneration, lack of biomarkers for premotor stage of PD and inadequate drug delivery across blood–brain barrier. Solutions for these challenges will be warranted for future studies with novel antioxidative treatment in PD patients.

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Effects of Safinamide on Motor Complications and Pain in Advancing Parkinson’s Disease – Post Hoc Analyses of Pivotal Trials

European Neurological Review ◽

10.17925/enr.2015.10.02.176 ◽

2015 ◽

Vol 10 (2) ◽

pp. 176 ◽

Cited By ~ 2

Author(s):

Ubaldo Bonuccelli ◽

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Water Soluble ◽

European Medicines Agency ◽

Motor Symptoms ◽

Motor Complications ◽

Neuronal Systems ◽

Post Hoc ◽

Dual Mechanism ◽

Non Motor Symptoms

Chronic levodopa (l-dopa) treatment of Parkinson’s disease (PD) patients is associated with motor complications (fluctuations and dyskinesias), which limit l-dopa efficacy and require drug therapy adjustments. Moreover, patients often experienced many non-motor symptoms, such as pain, which have a major impact on their quality of life. The neuropathology of PD has shown that complex, interconnected neuronal systems, regulated by a number of different neurotransmitters in addition to dopamine, are involved in the aetiology of motor and non-motor symptoms. Safinamide is a water-soluble, orally active aminoamide derivative that modulates dopaminergic and glutamatergic neurotransmission with a new and unique dual mechanism of action. Safinamide has been recently approved by the European Medicines Agency for the treatment of fluctuating PD patients as add-on therapy to l-dopa alone or in combination with other antiparkinson drugs. This article summarises the results of thepost hocanalyses of the long-term efficacy of safinamide on motor complications and pain performed in three pivotal clinical trials.

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