Effects of Coenzyme Q10 on Charcot-Marie-Tooth Disease
The object of this research is to test the effectiveness of Coenzyme Q10 (CoQ10) on symptoms of weakness, fatigue, and pain in persons with Charcot-Marie-Tooth disease (CMT).In this study we also intend to examine the impact of daily supplementation on overall quality of life.We are also interested in identifying any differences in serum ratios of CoQ10 in the oxidized and reduced forms.
CoQ10 is an integral part of the electron transport chain in the mitochondria, or the energy production centers of cells. Within recent years, there has been expanding interest in the potential benefits of CoQ10 supplementation on a variety of neuromuscular diseases, some of which involve mitochondrial dysfunction, such as CMT. Daily supplementation may have cytoprotective and neuroprotective properties, which may improve symptoms of weakness, fatigue, and pain, as well as increase quality of life (QOL) among persons with CMT.
With regards to within group comparisons we hypothesize that daily supplementation of CoQ10 taken as a 300 milligram wafer twice a day for 3 months will produce a statistically significant reduction in weakness, fatigue, and pain, along with a significant improvement in QOL as indicated from scores in both standardized physiological and scale measures.
The addition of serum level analysis will help to contextualize clinical results. We hypothesize the ratios of the oxidized and reduced forms of CoQ10 will be modified upon supplementation.
Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Efficacy Study, Intervention Model: Crossover Assignment, Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor), Primary Purpose: Supportive Care
Charcot Marie Tooth Disease
Coenzyme Q10, Coenzyme Q10
John P Murtha Neuroscience and Pain Institute
Memorial Medical Center
Results (where available)
- Source: http://clinicaltrials.gov/show/NCT00541164
- Information obtained from ClinicalTrials.gov on July 15, 2010
The study is aimed to test the hypothesis that there is anticipation in CMT
Charcot-Marie-Tooth type IA (CMT1A) is the most prevalent hereditary peripheral neuropathy. Demyelination of peripheral nerves is the hallmark of CMT1A. Ascorbic acid has been shown to hav...
This study was designed to evaluate the symptomatic effects of Coenzyme Q10 nanodispersed solution in middle-stage Parkinson's disease (PD) patients (Hoehn&Yahr II to III). The treatment p...
The purpose of this study is to compare the effects of varying dosage of coenzyme Q10 (CoQ10) versus a placebo in the treatment of Parkinson's disease (PD) in patients with early, untreate...
This research study hopes to examine the effects of Coenzyme Q10 on doxorubicin (Adriamycin) metabolism during breast cancer treatment. Doxorubicin is a lifesaving breast cancer treatment....
Charcot-Marie-Tooth disease is an inherited neuropathy causing progressive weakness, foot deformity and difficulty walking. Clinical anecdotes suggest orthoses designed on the 'sensorimotor' paradigm ...
To explore and describe the perceived facilitators and barriers to physical activity and examine the physical activity correlates in people with Charcot-Marie-Tooth disease.
To explore the clinical features of a novel glycyl-tRNA synthetase (GARS) gene mutation in a family with Charcot-Marie-Tooth disease type 2D (CMT2D).
Inherited peripheral neuropathies are among the most common genetic neuromuscular disorders worldwide. However, their diagnosis can be challenging due to genotypic and phenotypic variability. Charcot-...
Charcot-Marie-Tooth (CMT) disease is a common neurogenetic disorder and its heterogeneity is a challenge for genetic diagnostics. The genetic diagnostic procedures for a CMT patient can be explored ac...
Medical and Biotech [MESH] Definitions
S-Acyl coenzyme A. Fatty acid coenzyme A derivatives that are involved in the biosynthesis and oxidation of fatty acids as well as in ceramide formation.
An early growth response transcription factor that controls the formation of the MYELIN SHEATH around peripheral AXONS by SCHWANN CELLS. Mutations in EGR2 transcription factor have been associated with HEREDITARY MOTOR AND SENSORY NEUROPATHIES such as CHARCOT-MARIE-TOOTH DISEASE.
A coenzyme A derivative which plays a key role in the fatty acid synthesis in the cytoplasmic and microsomal systems.
A ferredoxin-containing enzyme that catalyzes the COENZYME A-dependent oxidative decarboxylation of PYRUVATE to acetyl-COENZYME A and CARBON DIOXIDE.
A hereditary motor and sensory neuropathy transmitted most often as an autosomal dominant trait and characterized by progressive distal wasting and loss of reflexes in the muscles of the legs (and occasionally involving the arms). Onset is usually in the second to fourth decade of life. This condition has been divided into two subtypes, hereditary motor and sensory neuropathy (HMSN) types I and II. HMSN I is associated with abnormal nerve conduction velocities and nerve hypertrophy, features not seen in HMSN II. (Adams et al., Principles of Neurology, 6th ed, p1343)