Study: Rumoring Coenzyme Q10 in Parkinson's disease

Von Natur.wiki Autoren-Team

Referenz Yoritaka A., Kawajiri S., Yamamoto Y., et al. Randomisierte, doppelblinde, placebokontrollierte Pilotstudie mit reduziertem Coenzym Q10 bei Parkinson. Parkinsonismus Relat Disord. 2015;21(8):911-916. Design Randomisierte, doppelblinde, placebokontrollierte Pilotstudien mit parallelen Gruppen Teilnehmer Japanische Patienten mit einer aktuellen Diagnose der Parkinson-Krankheit (PD). Die Teilnehmer wurden in 2 parallele Gruppen eingeteilt. Gruppe A umfasste diejenigen, die mit Levodopa behandelt wurden und bei denen „Wearing-off“-Effekte (dh frühes Auftreten von PD-Symptomen vor der nächsten planmäßigen Medikamentendosis) auftraten. Gruppe B umfasste diejenigen mit einer frühen Diagnose, die Levodopa noch nicht einnahmen, obwohl andere Medikamente erlaubt waren. An den Studienendpunkten hatte Gruppe A 14 auswertbare Teilnehmer …
Reference Yoritaka A., Kawajiri S., Yamamoto Y., et al. Randomized, double -blind, placebo -controlled pilot study with a reduced coenzyme Q10 at Parkinson's. Parkinsonism relat disord. 2015; 21 (8): 911-916. Design randomized, double-blind, placebo-controlled pilot studies with parallel groups participants Japanese patients with a current diagnosis of Parkinson's disease (PD). The participants were divided into 2 parallel groups. Group A included those treated with Levodopa and in which "Wearing-Off" effects (i.e. early occurrence of PD symptoms appeared before the next scheduled drug dose). Group B included those with an early diagnosis that Levodopa did not yet take, even though other medication were allowed. At the end of the study, Group A had 14 evaluable participants ... (Symbolbild/natur.wiki)

Reference

Yoritaka A., Kawajiri S., Yamamoto Y., et al. Randomized, double -blind, placebo -controlled pilot study with a reduced coenzyme Q10 at Parkinson's. Parkinsonism Relat Disord . 2015; 21 (8): 911-916.

Design

randomized, double -blind, placebo -controlled pilot studies with parallel groups

participant

Japanese patients with a current diagnosis of Parkinson's disease (PD). The participants were divided into 2 parallel groups. Group A included those treated with Levodopa and in which "Wearing-Off" effects (i.e. early occurrence of PD symptoms appeared before the next scheduled drug dose). Group B included those with an early diagnosis that Levodopa did not yet take, even though other medication were allowed. At the end of the study, Group A had 14 participants in the intervention group and 12 in the placebo group. Group B had 14 participants in the intervention group and 8 in the placebo group.

Intervention

Reduced Coenzyme Q10 (ubiquinol-10, 300 mg/day) or placebo, taken twice a day than 3 capsules. Each capsule contained 50 mg ubiquinol-10, 68.31 mg glycerin fatty acid ester, 0.3 mg lecithin, 154.39 mg rapeseed oil and 22 mg beeswax. Placebo contained everything except 50 mg ubiquinol. Group A received ubiquinol-10 or placebo for a total of 48 weeks and group B a total of 96 weeks.

target parameter

The Total Unified Parkinson's Disease Rating Scale (UPDRS) was used to pursue functional deficits from PD. The evaluation was carried out at the beginning of the course and in weeks 8, 24 and 48 and 8 weeks after the intervention for group A. The participants in group A were rated both in their "An" and in their "AUS" phase. Group B was assessed at the beginning of the course and in weeks 8, 24, 48 and 96 and 8 weeks after the intervention was terminated.

important knowledge

Group A: UpDRS scores sank (-4.2 +-8.2) for the ubiquinol 10 group and climbed (2.9 = -8.9) for the placebo group. This difference was statistically significant ( p < 0.05). There were no significant changes in the time of the "An" and "Aus" phases. There were significant differences in the subscores for finger and hand movements ( p < 0.05). However, there were no significant differences in tremor, stiffness, pounding of the foot, which resulted from a chair, posture, gait or immobility. Improvements were not maintained 8 weeks after stopping ubiquinol-10.
Group B: There were no significant differences in the overall UPDRS values ​​between the intervention and placebo arms. There was no significant changes in the subscores at any time or 8-week post-intervention assessment.
Supplementation with ubiquinol-10 increased the mirrors of the circulating Coenzyme Q10 in both groups, about 10 times. The COQ10 levels no longer correlated with any changes in symptoms.

practice implications

PD is a progressive disease and established drug treatments can prevent the disease process, but cannot stop. In 2002 a small study, the QE2 study, excited excitement by pointing out that the intake of 1,200 mg COQ10 per day (as Ubichinon-10 + alpha-tocopherol) people with earlier PD could benefit. the up to 2,400 mg/day Ubichinon + alpha-tocopherol, canceled prematurely due to lack of use (median studies 10.4 months). The results of QE3 were published in 2014. 2 In the meantime between the QE2 and QE3 studies, smaller studies with Ubichinon-10 also showed no use in the early Parkinson's disease.
The current pilot study is the first to use the reduced form of COQ10 (ubiquinol-10) in patients with Parkinson's. It indicates that ubiquinol-10 can alleviate some of the symptoms of Parkinson's disease in patients with “wear” by Levodopa. However, there was no improvement in patients with an early diagnosis who did not yet take a levodopa. Although this study is too small to create final clinical guidelines, it raises persistent questions whether Coenzyme Q10 is recommended and if so, what form is the best.
The pathogenesis of PD has long been suspected of impairment/loss of energy production in the mitochondrial respiratory chain in general and complex I in particular. 5 Early research implied damage by free radicals as the cause of this, since they are always available and in the neurons of the nigra nigra at PD. The damage to neurons by free radicals is clearly involved in neurodegeneration, but whether free radicals are caused or associative remains controversial.
This more complicated pathophysiology in Parkinson's could explain why a simple increase in Coenzyme Q10 is not sufficient to measure the progression of the disease measurably.
The basic idea behind the use of Coenzyme Q10 at Parkinson's was to support the energy production of complex I and act as antioxidants to prevent damage from the outset. This appeared logical, especially in connection with ongoing clinical data, which show that a lack of COQ10 occurs frequently in patients with Parkinson's. 7 We now know that the dysfunction of mitochondria in neurodegenerative diseases is much more complicated than previously assumed. The latest data indicates that the dysfunction of mitochondria is a highlight of many possible cellular aberrations, including mutations in mitochondrial DNA (MTDNA), mutations in nuclear genes that regulate the MTDNA or mitochondrial proteins, and misconception of important mito -ochondrial proteins at PD). 8.9 This more complicated pathophysiology in Parkinson's could explain why a simple increase in Coenzyme Q10 is not sufficient to meet the progression of the disease measurably.
The current study suggests that ubiquinol-10 could have a positive effect on those who already take Levodopa. However, the results for patients with Parkinson's early stages match the most earlier findings for Ubichinon-10. High -dose COQ10 does not slow down the progression of the disease. Larger studies are required to determine whether the results of this current pilot study can be replicated to those whose Levodopa effect "subsides".
Ubinquinol-10 is reduced COQ10 and ubiquinon-10 is the oxidized form. The mutual conversion between these molecules is easily achieved by redox flow. However, 95 % of the circulating COQ10 are in the reduced state, ubiquinol-10, regardless of which form is administered orally. 10 The oral absorption of ubiquinol-10 seems to be superior to 3 to 4 times. Provide ubiquinol in low-dosed shapes, usually 50-100 mg/capsule. The study currently reviewed here also compensates for this difference by using only 300 mg/day ubiquinol-10 compared to up to 2,400 mg/day ubiquinon-10, which was used in other PD studies.
From a practical point of view, the costs for high -dose COQ10, either as a ubiquinol or ubiquinone, are difficult to justify in view of the previous evidence of patients with Parkinson's in the early stage. A dose that ensures that the patient has no defect is careful given the likelihood of a defect in PD. It is still open whether the ideal form is ubiquinol or ubichinon, since both forms lead to increased ubiquinol in plasma.

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