Category: Children

Coenzyme Q and autoimmune diseases

Coenzyme Q and autoimmune diseases

Diseasez Betoptic Clenzyme CoQ10 supplements may reduce the heart-related side effects of betaxolol drops Cornzymea beta-blocker Positive body image used autoiimmune treat uatoimmune, without making the Coenzyme Q and autoimmune diseases diseased less diseasee. Systematic review of effect of coenzyme Q10 Coenzyme Q and autoimmune diseases physical exercise, hypertension Supplementation for sports performance heart failure. Too Natural health products free radicals diseasess the body can contribute to cellular and DNA damage as well as chronic inflammation, which can lead to a variety of inflammatory health conditions such as heart disease, autoimmune conditions, and even cancer. CoQ10 is a powerful weapon preventing the generation of free radicals and reactive oxygen species ROSwhich are associated with oxidative damage, immune impairment, and chronic degenerative diseases. Singh G, Athreya BH, Fries JF, Goldsmith DP. CoQ10 also exhibited immunomodulatory effects on B and T-cells, such as down-regulating IL expression and Th17 cells population induced by inflammatory response. Effects of coenzyme Q10 on the heart ultrastructure and nitric oxide synthase during hyperthyroidism. Coenzyme Q and autoimmune diseases

Coenzyme Q and autoimmune diseases -

The cJADAS is computed by assessing the following variables:. The Childhood Health Assessment Questionnaire CHAQ assesses functional ability in 8 domains of physical function 30 items for children dressing and grooming, arising, eating, walking, hygiene, reach, grip, and activities.

Each item is scored on a four-point scale ranging from 0 without any difficulty , 1 with some difficulty , 2 with much difficulty , 3 unable to do. The mean score of the eight domains finally makes up the disability index and ranges from 0 no disability to 3 disabled. Quality of life scores will be performed for patients at baseline and at the end of the 3-months trial period.

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For general information, Learn About Clinical Studies. Layout table for eligibility information Ages Eligible for Study: 3 Years to 16 Years Child Sexes Eligible for Study: All Accepts Healthy Volunteers: No Criteria Inclusion Criteria:.

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Home Search Results Study Record Detail Saved Studies. Save this study. Warning You have reached the maximum number of saved studies Coenzyme Q10 in Juvenile Idiopathic Arthritis Patients The safety and scientific validity of this study is the responsibility of the study sponsor and investigators.

Listing a study does not mean it has been evaluated by the U. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating.

Read our disclaimer for details. gov Identifier: NCT Recruitment Status : Recruiting First Posted : May 23, Last Update Posted : May 31, See Contacts and Locations.

View this study on the modernized ClinicalTrials. Study Details Tabular View No Results Posted Disclaimer How to Read a Study Record. Study Description. Go to Top of Page Study Description Study Design Arms and Interventions Outcome Measures Eligibility Criteria Contacts and Locations More Information.

Show detailed description. Hide detailed description. Detailed Description:. Sixty patients will be recruited in the study and will be randomized to one of the following groups: A Intervention Coezyme Q10 Group 30 patients : will receive their JIA standard treatment plus mg Coenzyme Q10 capsules daily for 3 months.

B Control Group 30 patients : will receive their standard JIA treatment plus placebo Blood samples will be withdrawn from patients at baseline and at the end of the 3 months trial period. Resource links provided by the National Library of Medicine MedlinePlus Genetics related topics: Juvenile idiopathic arthritis.

MedlinePlus related topics: Arthritis Juvenile Arthritis. Drug Information available for: Ubidecarenone. FDA Resources. Arms and Interventions. Coenzyme Q10 soft gelatin capsules daily for 3 months. Patients will receive their standard JIA treatment plus placebo.

Outcome Measures. Primary Outcome Measures : Disease Activity Evaluation [ Time Frame: 3 months ] Clinical efficacy will be assessed by calculating the Clinical Juvenile Arthritis Disease Activity Score cJADAS at baseline and at the end of the 3-month trial period.

Secondary Outcome Measures : Serum Malondialdehyde [ Time Frame: 3 months ] an oxidative stress markers, Malondialdehyde MDA will be assessed form patients sera at baseline and after 3 months. It will be measured using ELISA Kits.

serum samples will be withdrawn from each patient at baseline and after 3 months. Tumor necrosis factor-alpha will be measured using an ELISA Kit. CoQ10 safety will be monitored by asking the parents through interviews and phone calls every 2 weeks about the occurrence of any of the following side effects: abdominal discomfort, loose stools, headache, nausea, and vomiting.

assessment will be done every 2 weeks. an oxidative stress markers, glutathione will be assessed form patients sera at baseline and after 3 months. Eligibility Criteria. Layout table for eligibility information Ages Eligible for Study: 3 Years to 16 Years Child Sexes Eligible for Study: All Accepts Healthy Volunteers: No Criteria.

Patients with peripheral oligo or polyarthritis. With more than 6-month disease duration Participants who have inadequate response to at least one first line standard therapy.

Patients who have been receiving a stable treatment regimen for the past 3 months Exclusion Criteria: Patients with active systemic JIA Patients presenting with complications such as amyloidosis, uveitis, or glomerulonephritis Patients with other chronic autoimmune disease.

Contacts and Locations. Information from the National Library of Medicine To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor. Please refer to this study by its ClinicalTrials. gov identifier NCT number : NCT Layout table for location contacts Contact: Nourhan N Elsherif nourhan.

nasser18 pharma. Layout table for location information Egypt Pediatric Allergy, Immunology, Rheumatology Clinic, Children's Hospital, Ain Shams University Hospital Recruiting Cairo, Egypt.

More Information. Publications: Prakken B, Albani S, Martini A. Juvenile idiopathic arthritis. doi: Inflammation is the root cause of most illness these days, and luckily, CoQ10 has shown 2 an ability to reduce levels of the inflammatory compounds CRP and TNF-a as well as the pro-inflammatory cytokine IL-6 3.

This is most likely due to its ability to inhibit production of the one inflammatory protein in particular, called NF-kB. This autoimmune disease affects millions of Americans and is characterized by chronic inflammation and pain throughout the body.

In cases of fibromyalgia, CoQ10 is unevenly distributed 4 throughout the body which contributes to higher oxidative stress - which is important since increased oxidative stress is a contributor to inflammation and chronic pain. This makes regular supplementation important for those struggling with this condition.

Heart disease is one of the leading causes of death in America — and it is also intricately connected to lifestyle factors like diet, exercise, and smoking and alcohol consumption.

Researchers have looked into the effects of CoQ10 supplementation and its ability to significantly improve 5 heart health. Depression is the leading cause of disability in the U.

CoQ10 is a great supplement for a wide range of health woes. If you struggle with any of the issues mentioned above, talk to your doctor or health practitioner about CoQ10 — it might just make the difference!

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Our content may include products that have been independently chosen and recommended by Dr. Will Cole and our editors. If you purchase something mentioned in this article, we may earn a small commission. Will Cole, DNM, IFMCP, DC is a leading functional medicine expert who consults people around the globe, starting one of the first functional medicine telehealth centers in the world.

Named one of the top 50 functional and integrative doctors in the nation, Dr. Will Cole provides a functional medicine approach for thyroid issues, autoimmune conditions, hormonal imbalances, digestive disorders, and brain problems.

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Email Address. Is CoQ10 Right For You? ARTICLE CONTINUES BELOW. Email Address Required. CoQ10 The basics I frequently lean on CoQ10 — which stands for coenzyme Q10 — because it can elevate certain areas of health that many of my patients struggle with.

The ubiquinone therapeutic effectiveness has been reported in many diseases affecting this pathogenetic factor Chan et al. Ubiquinol is the reduced form of CoQ10, associated with antioxidant function.

Hence, the tissues and cells should have molecular mechanisms to recover their active form, including the dihydroorotate dehydrogenase action in the IMM, causing pyrimidine biosynthesis and reducing ubiquinone through the oxidation of dihydroorotate to rotate.

Also, its tail contains ten isoprenyl chemical subunits Matthews et al. CoQ10 is a crucial cofactor to produce ATP in the electron transport chain ETC Manzar et al. This coenzyme delivers electrons from complexes I and II and transfers them to complex III Alcázar-Fabra et al.

Moreover, an increase in the expression of mitochondrial uncoupling proteins UCPs demonstrates the antioxidant role of CoQ10 Persson et al. CoQ 10 as an important endogenous antioxidant is a crucial component of the mitochondrial respiratory chain MRC.

Such a CoQ-free pool can be applied by enzymes linking the MRC to other pathways, like the fatty acid β-oxidation and amino acid catabolism, pyrimidine de novo biosynthesis, proline, arginine, and glyoxylate metabolism, glycine metabolism, and sulfide oxidation metabolism that some of them are attached to metabolic pathways in other compartments Pradhan et al.

The antioxidant function of CoQ10 is because of its completely reduced ubiquinol form. Thus, a CoQ10 deficiency can cause some diseases due to a failure in energy metabolism and compromising cellular antioxidant capacity. Several diseases are caused by CoQ10 deficiency, such as heterogeneous MRC disorders.

Defects in cellular CoQ10 status are due to its primary or secondary deficiency Neergheen et al. Based on these findings, the antioxidant impact of the CoQ10 declines the function of inflammatory factors evidenced by gene expression analysis as well as cell culture assessments Hargreaves, The robust neuroprotective effects of the CoQ10 on neurotoxicity have been shown in many in vitro investigations and also animal models of neurological diseases Spindler et al.

AD is also known as the prevalent type of dementia Wang et al. Deficits in memory and learning, defects in thinking, and behavioral signs are the symptoms of dementia Alzheimer's Association, ; Shekarian et al.

Recently, genetic Picone et al. The accumulation of Aβ senile plaques plays an important role in AD pathogenesis Golde et al. It Presenilin 1 PS-1 mutation LP: proline by leucine substitution at codon causes the formation of Aβ42 and Aβ40 in the brains of transgenic mice and cultured cells Borchelt et al.

Therefore, CoQ10 might be a therapeutic candidate for the treatment of AD Yang et al. According to in vitro investigations, Aβ induces oxidative stress. For instance, Aβ increases the hydrogen peroxide H2O2 and lipid peroxide concentrations in cultured cells, and antioxidants, like vitamin E with a protective role in neurons against Aβ-related cytotoxicity Chan and Shea, Oxidative stress can cause aging and results from the imbalance between oxidants and antioxidants Wang et al.

Accordingly, oxidative stress causes AD Markesbery, ; Santos et al. Both mitochondrial dysfunction and oxidative damage lead to Aβ deposition in AD Beal, CoQ10 is capable of scavenging free radicals Gazdík et al. The synthesis of CoQ10 is diminished in older people Borek, CoQ10 inhibited apoptotic death and damage caused by ROS Li et al.

in corn oil in AD rats reduced thiobarbituric acid reactive substances TBARS and elevated the activity of antioxidant enzymes in the brain Ishrat et al. Treatment of hypercholesterolemia rats with Co-Q10 alone or in combination with omega-3 1, mg regulated cholinergic functioning, reduced brain inflammation and oxidative stress, and increased the functional outcome verified through the histopathological evaluation of brain tissues Ibrahim Fouad, The synaptic mechanisms of learning and memory in vertebrates are studied by long-term potentiation LTP of the hippocampal synaptic transmission Bliss and Collingridge, The long-term synaptic plasticity in the hippocampus HIP is suppressed by Aβ peptides Chen et al.

Figure 2. Oxidative stress and mitochondrial dysfunction lead to the formation of β-amyloid Aβ senile plaques. Deposition of Aβ increases the activity of acetylcholinesterase AChE. Also, oxidative stress leads to apoptosis and memory impairment by activating glial cells. The antioxidant and anti-apoptotic effects of CoQ10 improve memory.

AIF, apoptosis-inducing factor; AchE, acetylcholinesterase. The administration of CoQ10 alone or in combination with other antioxidants improved learning and memory and prevented oxidative stress, inflammation, and cellular death in various models of AD and frontotemporal dementia, including aged rodents with aluminum-induced AD, rats with forebrain lesions, rats receiving ICV infusion of Aβ or STZ, transgenic mice with different mutations inducing AD or frontotemporal dementia, and cell cultures using different human or rodent cells Jiménez-Jiménez et al.

Initial short-term randomized clinical trials have shown an improvement in several neuropsychological tests in AD patients treated with CoQ10 in comparison with those receiving the placebo due to the potential effectiveness of CoQ10 Weyer et al.

A systematic review was conducted to examine the possible therapeutic effects of CoQ10 in experimental models of AD and other dementias, as well as in humans with AD and mild cognitive impairment.

The potential role of CoQ10 treatment in AD and improving memory in aged rodents in experimental models deserves future studies on patients with AD through the assessment of other causes of dementia and mild cognitive impairment Jiménez-Jiménez et al.

Depression as a neurological disorder is caused by the lack of serotonin Anderson and Maes, Lower serotonin levels can be a major outcome of tryptophan metabolism shift to kynurenine formation Caspi et al.

In tryptophan oxidation, indoleamine 2, 3-dioxygenase 1 IDO 1 is a rate-limiting enzyme. The tryptophan-to-kynurenine conversion plays a role in the development of depression Dantzer et al. Most people experience repeated episodes of mood disorders, psychosocial morbidity, and high use of healthcare services, which persist into later life Bartels et al.

Bipolar depression is the significant and least effectively treated stage of bipolar disorder BD. In BD, the proportion of the time spent in depressive episodes is more than the time spent in manic episodes Forester et al.

Treatment of BD has not been widely considered and also treating depressive symptoms is not easily achievable in the manic stage Konradi et al. Lower plasma CoQ10 concentrations in depressed patients were compared with healthy controls Maes et al.

Also, CoQ10 is effective in the pathophysiology of many disorders linked to depressive symptoms, like fibromyalgia FM , major depression, and myalgic encephalomyelitis Forester et al.

The results showed improved depressive symptoms compared to cases treated with the placebo Alcocer-Gómez et al. Mitochondrial dysfunction, oxidative stress, and inflammation are involved in the BD pathophysiology. Inflammatory responses, such as elevated leucocyte and neutrophil counts and plasma concentrations of proinflammatory cytokines and their receptors are found in cases of severe depression.

On the other hand, major depression is linked to reduced antioxidant levels as well as induced nitrosative and oxidative pathways Maes et al. ROS, like hydroxyl radical, superoxide, H2O2, and peroxynitrite, are effective in the pathogenesis of major depression Lucca et al.

It CoQ10 plays a role in depression pathophysiology through the anti-inflammatory and neuroprotective properties and suppresses the generation of pro-inflammatory cytokines Schmelzer et al.

Reduced levels of CoQ10 are associated with an elevated level of tumor necrosis factor-alpha TNF-α and oxidants, such as ROS Schmelzer et al. The suppressed neuro-inflammatory response in the prefrontal cortex PFC and HIP was observed, evidenced by reduced NF-kB, p38, and JNK concentrations in the CoQ 10 groups Salehpour et al.

Moreover, the CoQ10 antioxidant effect was exhibited by its capability to significantly decrease elevated hippocampal 4-hydroxynonenal and MDA levels and increase the decreased catalase and glutathione levels. Furthermore, CoQ10 caused a significant reduction in the levels of different pro-inflammatory cytokines, such as interleukin-1β IL-1β , IL-2, IL-6, and TNF-α Abuelezz et al.

Therefore, CoQ10 due to its anti-inflammatory and anti-oxidative effects can be used to treat depression. Figure 3. The effects of CoQ10 on depression by inhibiting inflammation and stress oxidative pathways.

A significant difference was found between the depression induced by streptozotocin STZ and control groups tested by the splash test and FST 24 h after STZ treatment.

In addition, according to the validated and accurate high-performance liquid chromatography HPLC , reduced CoQ 10 levels were found in the brain of the STZ group Andalib et al.

Epilepsy is the commonest neurological disease worldwide, in which spontaneous unusual electrical discharges of neurons are observed throughout the brain Patel, Temporal lobe epilepsy TLE is the commonest form of epilepsy in adults that is commonly linked to hippocampal sclerosis, neurodegeneration, and hippocampal circuit reorganization Jokeit and Schacher, An animal model of TLE was designed by unilateral intrahippocampal kainic acid injection in rodents.

These models are used to study the effects of possible antiepileptic agents because in the time interval between the status and the first spontaneous seizures, we can examine the effect of neuroprotective and prophylactic agents on epilepsy Sharma et al.

Epilepsy approximately affects 0. Contrary to the prevalence of recent effective antiepileptic agents in cases with epilepsy, novel antiepileptic agents are used with stronger anticonvulsant activity Sattarinezhad et al.

Therefore, new therapeutic strategies have been established to prevent or even reverse the molecular and cellular mechanisms of epileptogenesis Löscher and Schmidt, CoQ10 caused a reduction in the kainate-related model of epilepsy Yalcin et al.

CoQ10 has anti-apoptotic and antioxidant effects Papucci et al. Moreover, CoQ10 0. The neuroprotective properties of CoQ10 i. Nitric oxide NO is a regulator of seizure activity because of its various anticonvulsant Starr and Starr, ; Theard et al.

Also, CoQ10 1. However, the oxidized low-density lipoprotein-associated down-regulation of eNOS is declined by CoQ10 Tsai et al. In addition, this coenzyme, dissolved in corn oil, increases the aortal eNOS activity in acrylonitrile-related vascular endothelial abnormalities in rats Guo et al.

Therefore, the effect of CoQ10 on seizure was attenuated by the NOS inhibitor. Furthermore, based on the electrophysiological evidence, CoQ10 administration increased the absence seizures through the stimulation of the neuronal NOS Gunes et al.

Therefore, the inhibition of NOS decreased the seizure activity of CoQ This antiseizure effect of subchronic CoQ10 was attenuated by the NOS inhibitor Sattarinezhad et al.

Therefore, the interaction between NO and subchronic CoQ10 in antiseizure activity is possibly accomplished by the induction of NOS. Basically, non-inflammatory mechanisms, such as mitochondrial dysfunction cause MS Kalman et al.

Free radicals play a role in MS pathogenesis and enhance the transendothelial migration of leukocytes resulting in oligodendrocyte injury and axonal degeneration Van Horssen et al. Macrophages produce free radicals, including NO, ROS, reactive nitrogen species, microglia, and astrocytes, which all damage the neurons, axons, myelin, and oligodendrocyte Lee et al.

Figure 4. Inflammation, neuronal demyelination, mitochondrial dysfunction, destruction of axons and oligodendrocytes, and oxidative stress are the main pathological causes of multiple sclerosis MS.

CoQ10 improves the disease by reducing the activity of microglia and macrophages and the production of reactive oxygen species ROS. Also, inflammation, multifocal demyelination, loss of oligodendrocytes, breakdown of the blood-brain barrier BBB , neural and axonal injury, and oxidative stress are the causes of MS Van der Walt et al.

Inflammatory markers, ROS, and matrix metalloproteinases MMPs , as the factors to enhance BBB permeability, can be released by the infiltrated activated leukocytes in MS cases Larochelle et al.

Pro-inflammatory factors, like TNF-α, IL-1, IL-6, and interferon IFN -γ, increase the cerebrospinal fluid, serum, and brain lesions in MS cases.

They have relatively low concentrations of transforming growth factor-β and IL-4 Miller et al. Relapsing-remitting MS RRMS , progressive-relapsing MS, primary progressive MS, and secondary progressive MS are different MS types Adamczyk-Sowa et al.

RRMS is linked to immune-mediated reactions, like white matter inflammation, microglial activation, and cell infiltration in the CNS Van Horssen et al. The immune system plays a role in the development of depression associated with MS.

Pro-inflammatory cytokines, like TNF-α, induce weight loss, anorexia, anxiety, locomotor retardation, and reduced social exploration Kidd, Schmelzer et al. Fouad and Jresat prepared CoQ10 i. This antioxidant could reduce NF-κB and iNOS expression levels in the rats' livers Fouad and Jresat, CoQ10 enhances remyelination in the CPZ model Khalilian et al.

CoQ10 supplementation had no effect on GPx activity Sanoobar et al. PD is caused by the degradation of dopamine DA neurons in the SNpc. The symptoms of this disorder include resting tremors, postural instability, rigidity, and bradykinesia Colnat-Coulbois et al.

Although the causes of sporadic have not yet been discovered, different environmental risk factors, like neurotoxins can be involved Di Monte, Such neurotoxins inhibit complex I in the mitochondrial ETC. In normal circumstances, DA neurons also face a high level of oxidative stress because of ROS generation during DA metabolism Dexter et al.

ATP depletion and oxidative stress production cause neuronal death. Oxidative stress, activation of the microglia, neuroinflammation, mitochondrial damage, protein aggregation due to defective clearance, and autophagic stress are the major events in the pathophysiology of PD Kones, The disparity in mitochondrial dynamics causes augmentation of neuronal loss observed in PD patients Srivastava, One of the main non-motor symptoms of the disease is PD with mild cognitive impairment PDMCI.

The early identification of PDMCI and treatment of this disease are of critical importance to improve the quality of life and prognosis in PD patients Kwon et al. The levodopa-3,4-dihydroxyphenylalanine L-DOPA administration is the initial treatment for PD Nutt, Diminution of movement owing to delayed movement initiation akinesia is an important reason for disability in PD Lundblad et al.

L-DOPA pharmacotherapy can alleviate such symptoms. Moreover, prolonged treatments in the majority of patients lead to drug-induced abnormal involuntary movements dyskinesia Cenci, Currently, PD cannot be cured; however, neuroprotectants reduce the rate of neurodegeneration and improve the quality of life Koller and Cersosimo, CoQ10 has shown neuroprotective activity in some neurodegenerative diseases, like PD Mancuso et al.

Screening for oxidative stress markers in patients with neurodegenerative disease, such as PD showed lower CoQ10 concentrations and higher lipoprotein oxidation levels in the cerebrospinal fluid, plasma, and brain cortex than in non-affected cases. Affected patients showed an increase in the levels of mitochondrial oxidative stress due to low CoQ10 levels because CoQ10 administration could improve the clinical symptoms of some patients Jing et al.

Thus, antioxidants, like CoQ10 and vitamin E, are used in both preclinical investigations and clinical trials using animal models Shults et al. In a model of PQ-related neurodegeneration in male Long-Evans rats, the water-soluble CoQ10 [WS-CoQ10; 50 mg in PBS phosphate-buffered saline ] in drinking water was used to counteract the toxic effect of PQ.

PQ induction resulted in oxidative stress and the lack of DA neurons in SNpc, which can affect the motor skill of the animals during the rotarod test. Such PD-like behavioral symptoms showed an improvement in rats treated with WS-CoQ10 added to the drinking water Somayajulu-Nitu et al.

WS-CoQ10 is not natural but can be artificially prepared. The natural CoQ10 is lipid-soluble Parmar et al. Application of Ubisol-Q10 could remarkably offset the neurotoxicity and ameliorate motor impairment by MPTP Muthukumaran et al.

The combination of creatine and CoQ10 treated the MPTP-associated PD model in mice, suppressed the loss of neurons containing tyrosine hydroxylase in the SNpc, and also significantly decreased LPO damage and α-synuclein accumulation in the neurons of this area but did not improve the loss of the dopaminergic neurons Yang et al.

Accordingly, the elevated plasma level of CoQ10 following ingestion of the reduced form can be absorbed more effectively Cleren et al. Treatment with CoQ10 mg for 26 weeks showed a considerable improvement in oligoasthenoteratozoospermia outcomes, which was associated with mitochondrial dysfunction in male subjects Safarinejad et al.

Furthermore, in a double-blind study, about patients used CoQ10 at mg daily for 6 months. CoQ10 had few toxic effects on HD, but its long-term treatment and high dose did not reduce the symptoms of the disease McGarry et al. Furthermore, therapeutic interventions using CoQ10 in mice subjected to PQ 24 h following exposure , two times per week through 3 weeks, halted behavioral deterioration and ongoing neurodegeneration.

The outcomes of the sustained treatment with CoQ10 for 3 weeks were compared to L-DOPA as the standard drug of choice. CoQ10 caused a notable improvement in most of the behavioral tests and reduced protein carbonyl content in the brain, principally when it was started before rather than after PQ induction of PD.

In addition, water-soluble CoQ10 restored mitochondrial morphology and decreased fragmentation and consequently, mitochondrial fusion and improved mitochondrial dynamics, confirming the protective effect of CoQ10 against rotenone PD-mimicking toxin toxicity.

Thus, water-soluble CoQ10 can be used to treat PD and is effective in other diseases due to mitochondrial dysfunction Li et al. Therefore, CoQ10, which defends against mitochondrial damage, makes the progression of PD slow, mostly when started as prophylactic treatment Attia and Maklad, Figure 5.

CoQ10 has a neuroprotective effect against Parkinson's disease by inhibiting inflammation, oxidative stress, activation of microglia, protein accumulation, and mitochondrial damage.

Intrastriatal delivery of CoQ10 at a mean rate of 1. along with oral saline showed significant effectiveness in chlorpromazine -induced Parkinsonism-like alterations in mice Onaolapo et al. Patients with Lewy body dementia LBD showed decreased cerebellar cortex CoQ10 and those with progressive supranuclear palsy PSP had decreased CoQ10 levels in the cerebrospinal fluid Jiménez-Jiménez et al.

Neurodegenerative disorders, including PD Shults et al. According to Yang et al. Stroke is the third leading cause of mortality after heart disease and cancer. Three-quarters of stroke patients report an ischemic stroke, which can be due to blood vessel obstruction caused by a clot.

Considerable advances have been made in neuropharmacology, but the only clinically effective treatments are acetylsalicylic acid and tissue plasminogen activator Longa et al. Nonetheless, stroke-related mortality and morbidity rates are still high, and there is a need for the development of new treatments.

Inflammation, excitotoxicity, oxidative stress, and apoptosis necrosis, are the main factors associated with lesion progression after ischemia Ord et al. The efficacy of recanalization 3 h after limiting the onset of stroke symptoms has been approved in many patients.

Oxidative stress is the pathological mechanism of cerebral ischemia Rodrigo et al. Inhibition of antioxidants damages the structure and function of cells Simani et al. Therefore, nerve cells should be protected against oxidative stress Flint Beal and Shults, ; McCarthy et al.

MDA is the latest product of LPO that is increased in ischemic stroke patients depending on the infarct size, the stroke severity, and the patient's outcome Allen and Bayraktutan, Therefore, elevated concentrations of MDA in ischemic stroke patients have been reported in many studies Simani et al.

The decreased superoxide dismutase SOD activity in acute ischemic stroke has been observed in previous studies Cherubini et al.

This antioxidant enzyme, SOD, can reduce ROS levels Gupta et al. CoQ10 scavenges superoxide radicals for the production of oxygen and H2O2 Lee et al. Different cerebral ischemia models have shown promising therapeutic effectiveness for the constant administration of CoQ10 Obolenskaia et al.

However, the treatment of such urgent conditions, such as ischemic stroke should be performed with drugs through intravenous injections. The expression of genes associated with metabolism and intracellular signaling, embryogenesis, cell differentiation, and production of cholesterol and proinflammatory factors, including TNFα is affected by CoQ10 Groneberg et al.

UbiA prenyltransferase domain-containing protein 1 UbiAd1 is involved in CoQ10 generation and can catalyze the conversion of vitamin K1 into vitamin K2 Mugoni et al. Recently, the neuroprotective impact of vitamin K2 menaquinone isoform has been considered Shearer and Newman, Some treatments, including statin use, have been suggested for transient ischemic attack TIA Gargano et al.

Several experimental García-Bonilla et al. In other studies, the levels of blood CoQ10 in patients were reduced after the administration of atorvastatin Rundek et al. However, CoQ10 in the blood may disturb BBB following an ischemic insult. Atorvastatin exerts its degenerative effects through a decrease in CoQ10 and these effects are associated with the antioxidant-oxidant defense mechanism.

In an interventional study, serum CoQ10 levels significantly increased in the supplement-treated acute ischemic stroke AIS patients compared to the placebo group. Nonetheless, no significant difference was found in the Modified Ranking Scale score and MDA, SOD, and glial fibrillary acidic protein GFAP levels between the two groups Ramezani et al.

Molecular analysis has shown that primary mutations for this disease are point mutations in mitochondrial DNA mtDNA at positions 3,, 11,, and 14, Wallace et al. LHON can be associated with movement disorders, spastic paraparesis, cardiac arrhythmia, peripheral neuropathy, and skeletal abnormalities Shoffner et al.

Progressive visual loss with permanent centrocecal scotoma has been reported in most affected patients Lessell et al.

Some patients have symptoms, including ataxia, tremor, posterior column dysfunction, corticospinal tract dysfunction, dystonia, and extrapyramidal rigidity. LHON is associated with numerous neurologic disorders Chariot et al.

CoQ10 is effective in the treatment of patients with mitochondrial diseases, such as chronic progressive external ophthalmoplegia CPEO , Kearns-Sayre syndrome KSS , and other mitochondrial encephalomyopathies Ogasahara et al. CoQ10 caused a rapid improvement in visual acuity in these patients Kuo et al.

In another study, treatment was initiated with mg CoQ10 per day and multiple vitamins, including tocopherol mg , vitamin C mg , vitamin K3 10 mg , thiamine 10 mg , and riboflavin 10 mg. Gradual improvement in movement disorders occurred within a year.

Moreover, lesions of the subthalamic nuclei almost entirely disappeared Chariot et al. ARCA2 and SCAR9 is a kind of hereditary CoQ deficiency.

This rare ataxia is due to mutations in the aarF-domain-containing kinase 3 ADCK3 gene as an ortholog of yeast coq8 Lagier-Tourenne et al. ARCA2 is known for slow progressive gait impairment, exercise intolerance, cerebellar atrophy, epilepsy, and intellectual disability Mignot et al.

The deficiency of CoQ10 causes MRC disorder Hargreaves, A decrease in CoQ10 concentrations in tissues or cultured cells due to biallelic mutations in each of COQ2, COQ4, COQ6, COQ7, COQ8A, COQ8B, COQ9, PDSS1, and PDSS2 genes COQ genes involved in the CoQ10 biosynthesis can be observed in this kind of ataxia Emmanuele et al.

Patients with ADCK3 mutations experience a marked improvement following 3 weeks of oral supplementation with CoQ10 mg two times a day Shalata et al. The purpose of this article was to review the studies using experimental and clinical treatments Figure 7. Experimental treatments have often been studied in animal models with remarkable results.

In addition, clinical studies using a specific dose and duration of treatment have been effective. However, CoQ10 has no effect on some of the symptoms of the disease. The antidepressant effect of this neuroprotective agent has not yet been studied in patients with MS Sanoobar et al.

Also, in an animal study, contrary to the antioxidant effects of CoQ10, it led to an increase in the aortal eNOS activity in vascular endothelial abnormalities caused by acrylonitrile in rats Guo et al.

The neuroprotective properties of CoQ10 in the intrahippocampal kainate model of TLE have not yet been identified and more research is needed Baluchnejadmojarad and Roghani, In addition, long-term, high-dose CoQ10 therapy did improve the symptoms of HD McGarry et al.

In an intervention study on AIS patients, there were no statistically significant differences in the Modified Ranking Scale score, and MDA, SOD, and GFAP levels between the two placebo and supplement-treated groups Ramezani et al. A recent study on patients with LHON showed no changes in visual function after the administration of CoQ10 mg and other vitamins in the bilateral pallor of the optic disks Chariot et al.

According to the mentioned studies and their results, more relevant studies are needed in the future. CoQ10 as an antioxidant and neuroprotective agent can play a role in the treatment of neurological disorders.

Although neurological diseases cannot be treated effectively, CoQ10 deficiency is involved in the pathogenesis of epilepsy, stroke, MS, depression, PD, AD, LHON, ARCA2, and SCAR9.

More clinical and experimental studies are needed using electrophysiological and behavioral evaluation, genetic targeting, and molecular imaging.

SB, RH, SS, MK-A, AM, MR, and AK literature review and drafting the manuscript. SB and AK critically revision of the manuscript. All authors read and approved of the final manuscript. This study was supported by Hamadan University of Medical Sciences, Hamadan, Iran Grant No.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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Asistencia Sanitaria del SSPA. Coezyme - Hospital Universitario Reina Sofía. Therapeutic Potential and Immunomodulatory Role of Coenzyme Q10 and Its Analogues in Systemic Autoimmune Diseases. Simple item page. author López-Pedrera, Chary dc. author Villalba, José Manuel dc. Herbal fat metabolism blend Here to Order my aytoimmune book Gut Feelings. Diseaees you think the autlimmune, self-care, and autoimjune worlds diseasew overwhelming, just wait until you dive into the supplement industry. There are quite literally thousands Plant-based energizer capsules, Coenzyme Q and autoimmune diseases, tinctures, and tonics an choose from. There Coenzyme Q and autoimmune diseases adn, Coenzyme Q and autoimmune diseases, herbs, multis, and condition-specific blends — and of course, there are hundreds of brands, each claiming to be the best. Even as a functional medicine practitioner who is extremely well-versed in the supplement world, it still surprises me how much time it takes to keep up-to-date on all the research and science. By educating yourself on the importance of specific nutrients, you can better prioritize, starting with what makes the most sense for your body and specific health goals. One of the supplements I often find myself recommending to my patients in my functional medicine telehealth clinic is CoQ

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Coenzyme Q and autoimmune diseases -

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Share Facebook Twitter Linkedin Email Home Health Library. Coenzyme Q10 CoQ10; Ubiquinone. Uses Some studies suggest that coenzyme Q10 supplements, either by themselves or in with other drug therapies, may help prevent or treat the following conditions: After Heart Attack One clinical study found that people who took daily CoQ10 supplements within 3 days of a heart attack were less likely to have subsequent heart attacks and chest pain.

Heart failure HF There is evidence that CoQ10 may help treat heart failure when combined with conventional medications. High blood pressure Several clinical studies involving small numbers of people suggest that CoQ10 may lower blood pressure.

High cholesterol People with high cholesterol tend to have lower levels of CoQ10, so CoQ10 has been proposed as a treatment for high cholesterol, but scientific studies are lacking.

Diabetes CoQ10 supplements may improve heart health and blood sugar and help manage high blood pressure in people with diabetes. Heart damage caused by chemotherapy Several clinical studies suggest that CoQ10 may help prevent heart damage caused by certain chemotherapy drugs, adriamycin, or other athracycline medications.

Heart surgery Clinical research indicates that introducing CoQ10 prior to heart surgery, including bypass surgery and heart transplantation, can reduce damage caused by free radicals, strengthen heart function, and lower the incidence of irregular heart beat arrhythmias during the recovery phase.

Gum Periodontal disease Gum disease is a common problem that causes swelling, bleeding, pain, and redness of the gums. Other Preliminary clinical studies also suggest that CoQ10 may: Improve immune function in people with HIV or AIDS Increase sperm motility, improving male fertility Be used as part of the treatment for Parkinson disease Improve exercise ability in people with angina Help prevent migraines Scientific studies are needed to see whether CoQ10 can be safely and effectively used for these health problems and needs.

Dietary Sources Primary dietary sources of CoQ10 include oily fish such as salmon and tuna , organ meats such as liver , and whole grains.

Available Forms CoQ10 is available as a supplement in several forms, including soft gel capsules, oral spray, hard shell capsules, and tablets. How to Take It Pediatric DO NOT give CoQ10 to a child under 18 except under the supervision of a health care provider.

Adult For adults 19 years and older: The recommended dose for CoQ10 supplementation is 30 to mg daily. Precautions Because of the potential for side effects and interactions with medications, you should take dietary supplements only under the supervision of a knowledgeable health care provider.

Possible Interactions If you are being treated with any of the following medications, you should not use CoQ10 without first talking to your health care provider.

Study record managers: refer to the Data Element Definitions if submitting registration or results information. Juvenile idiopathic arthritis JIA is the most common chronic rheumatological disorder in childhood of unknown cause and a major cause of functional disability.

Standard JIA treatment including nonsteroidal anti-inflammatory drugs NSAIDs , corticosteroids, methotrexate, and biological agents have considerable adverse effects in addition to their high cost.

Despite the success of these treatment approaches, patients may still have active disease with other sequelae from chronic inflammation and considerable morbidity that may negatively impact patients' quality of life. Therefore, evaluating the potential benefit of alternative add-on anti-inflammatories and antioxidants might be a promising area for further research.

Coenzyme Q10 CoQ10 is a natural mitochondrial electron carrier and a powerful lipophilic antioxidant located in almost all cell membranes and plasma lipoproteins.

Several preclinical studies in animal models as well as clinical trials in adult patients with rheumatoid arthritis RA have demonstrated the beneficial effects of CoQ Results show that CoQ10 can reduce the oxidative and inflammatory status as well as clinical features that characterize this systemic autoimmune disease.

Also, CoQ10 has been used safely in children before and was well tolerated. Thus, the investigators would like to evaluate the effect of CoQ10 oral supplementation in pediatric JIA patients. Juvenile idiopathic arthritis JIA is the most common chronic rheumatological disorder in childhood of unknown etiology and a major cause of functional disability.

The American College of Rheumatology ACR defines JIA as inflammation in one or more joints of unknown etiology with onset prior to age 16 years and a minimum of 6 weeks duration, following the exclusion of other known causes of synovitis. The International League of Associations for Rheumatology criteria classifies JIA into several different subgroups depending on the number of joints affected, presence of extra-articular manifestations such as uveitis or glomerulonephritis, systemic symptoms, serology and genetic factors.

Peripheral arthritis is the common predominant clinical presentation among the various types. The three main types of JIA are polyarticular, oligoarticular, and systemic JIA. Therefore, diagnosis of JIA depends on physical findings, medical history, and the exclusion of other diagnoses.

The main hallmark of JIA is joint inflammation with bone resorption and tissue destruction. This chronic inflammation limits the daily activities and productivity of patients.

Interleukin-1 IL-1 , IL-6, IL, and tumor necrosis factor-α TNF-α are inflammatory cytokines that play an important role in the pathogenesis, prognosis, disease activity, and systemic features of JIA.

Additionally, abnormal activation of T-cells, B-cells, natural killer NK cells, dendritic cells DC , macrophages and neutrophils contribute to the pathogenesis of JIA.

All medications used to treat JIA including nonsteroidal anti-inflammatory drugs NSAIDs , corticosteroids, methotrexate, and biological agents have considerable adverse effects in addition to the high cost of the biologics.

Also, despite the success of these treatment approaches, patients may still have active disease with other sequelae from chronic inflammation and considerable morbidity that may negatively impact patients' quality of life.

Coenzyme Q10 CoQ10 is a mitochondrial electron carrier and a powerful lipophilic antioxidant located in almost all cell membranes and plasma lipoproteins. It can be found naturally and acquired from the diet or synthesized in-vivo by all cells of the body.

Various in-vitro and animal studies have demonstrated the antioxidant and anti-inflammatory effect of CoQ Several preclinical studies in animal models as well as clinical trials in patients with rheumatoid arthritis RA have demonstrated the beneficial effects of CoQ In an attempt to understand the mechanisms by which CoQ10 exerts its anti-inflammatory and immunomodulatory effect, Jhun et al conducted two studies on induced-arthritis mice models.

Their results showed that the mice that received CoQ10 showed significant decrease in RA severity. Immunohistochemical analysis of synovial tissue showed that CoQ10 administration lead to significantly lower levels of proinflammatory cytokines such as IL, IL-1, IL-6, IL, TNF-α and vascular endothelial growth factor VEGF.

Also, oxidative stress markers including nitrotyrosine and inducible nitric oxide synthase iNOS expression were significantly reduced in mice treated with CoQ CoQ10 also exhibited immunomodulatory effects on B and T-cells, such as down-regulating IL expression and Th17 cells population induced by inflammatory response.

Furthermore Bauerova et al. exhibited that the addition of CoQ10 to methotrexate MTX , the most commonly prescribed anti-rheumatic agent, suppressed the progression of RA in rats more than MTX alone. The effect on oxidative stress and immunomodulation was shown through a decrease in the plasma levels of MDA and IL-1, respectively.

This effect was shown in a study by Tawfik et al. where liver function enzymes improved after the combination of CoQ10 with MTX in rats. To further elucidate the effect of CoQ10 supplementation, two randomized clinical trials tested its use in adult rheumatoid arthritis patients.

Abdollahzad et al. focused on the effect of CoQ10 on oxidative stress and inflammatory markers. Moreover, no adverse drug events were observed confirming the safety and tolerability of CoQ With more focus on disease activity, Nachvak et al reported significant decrease in Disease Activity Scores DAS , swollen joint count, tender joint count, and the visual analogue scale VAS scores accompanied by a reduction in erythrocyte sedimentation rate ESR and matrix metalloproteinase MMP-3 levels.

Altogether, evidence supports the beneficial effect of CoQ10 supplementation not only on inflammatory markers and oxidative stress but also on clinical features and presentation of arthritis patients.

Up to date, there is no published study to evaluate the use of CoQ10 in JIA. Thus, the investigators would like to evaluate the effect of CoQ10 oral supplementation as adjuvant therapy on the clinical outcomes in pediatric JIA patients. A prospective, randomized, controlled, single blind clinical trial will be conducted on 60 Juvenile Idiopathic Arthritis JIA patients at the Pediatric Allergy, Immunology, Rheumatology Clinic, Children's Hospital, Ain Shams University.

At baseline, caregivers of patients who are eligible will be educated about the study protocol and will be required to sign a written informed consent before enrollment in the study. Sixty patients will be recruited in the study and will be randomized to one of the following groups:.

A Intervention Coezyme Q10 Group 30 patients : will receive their JIA standard treatment plus mg Coenzyme Q10 capsules daily for 3 months.

B Control Group 30 patients : will receive their standard JIA treatment plus placebo. Blood samples will be withdrawn from patients at baseline and at the end of the 3 months trial period. After 3 months of CoQ10 supplementation, all the outcomes will be reassessed and reported to determine the effect on CoQ10 supplementation.

Layout table for study information Study Type : Interventional Clinical Trial Estimated Enrollment : 60 participants Allocation: Randomized Intervention Model: Parallel Assignment Masking: Single Participant Masking Description: Placebo will be given to patients in the control group Primary Purpose: Treatment Official Title: The Effect of Coenzyme Q10 Supplementation on the Clinical Outcome of Juvenile Idiopathic Arthritis Patients Actual Study Start Date : May 1, Estimated Primary Completion Date : December Estimated Study Completion Date : December Resource links provided by the National Library of Medicine MedlinePlus Genetics related topics: Juvenile idiopathic arthritis MedlinePlus related topics: Arthritis Juvenile Arthritis Drug Information available for: Ubidecarenone U.

Dietary Supplement: Coenzyme Q10 Coenzyme Q10 soft gelatin capsules daily for 3 months Drug: Standard Regimen Patients may be receiving any of these commonly used JIA treatments including:. Patients may be receiving any of these commonly used JIA treatments including:. Clinical efficacy will be assessed by calculating the Clinical Juvenile Arthritis Disease Activity Score cJADAS at baseline and at the end of the 3-month trial period.

The cJADAS is computed by assessing the following variables:. The Childhood Health Assessment Questionnaire CHAQ assesses functional ability in 8 domains of physical function 30 items for children dressing and grooming, arising, eating, walking, hygiene, reach, grip, and activities.

Each item is scored on a four-point scale ranging from 0 without any difficulty , 1 with some difficulty , 2 with much difficulty , 3 unable to do. The mean score of the eight domains finally makes up the disability index and ranges from 0 no disability to 3 disabled.

Quality of life scores will be performed for patients at baseline and at the end of the 3-months trial period. Information from the National Library of Medicine Choosing to participate in a study is an important personal decision.

Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below.

For general information, Learn About Clinical Studies. Layout table for eligibility information Ages Eligible for Study: 3 Years to 16 Years Child Sexes Eligible for Study: All Accepts Healthy Volunteers: No Criteria Inclusion Criteria:.

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Home Search Results Study Record Detail Saved Studies. Save this study. Warning You have reached the maximum number of saved studies Coenzyme Q10 in Juvenile Idiopathic Arthritis Patients The safety and scientific validity of this study is the responsibility of the study sponsor and investigators.

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gov Identifier: NCT Recruitment Status : Recruiting First Posted : May 23, Last Update Posted : May 31, See Contacts and Locations.

View this study on the modernized ClinicalTrials. Study Details Tabular View No Results Posted Disclaimer How to Read a Study Record. Study Description. Go to Top of Page Study Description Study Design Arms and Interventions Outcome Measures Eligibility Criteria Contacts and Locations More Information.

Show detailed description. Hide detailed description. Detailed Description:. Sixty patients will be recruited in the study and will be randomized to one of the following groups: A Intervention Coezyme Q10 Group 30 patients : will receive their JIA standard treatment plus mg Coenzyme Q10 capsules daily for 3 months.

B Control Group 30 patients : will receive their standard JIA treatment plus placebo Blood samples will be withdrawn from patients at baseline and at the end of the 3 months trial period.

Resource links provided by the National Library of Medicine MedlinePlus Genetics related topics: Juvenile idiopathic arthritis. MedlinePlus related topics: Arthritis Juvenile Arthritis. Drug Information available for: Ubidecarenone. FDA Resources.

Arms and Interventions. Coenzyme Q10 soft gelatin capsules daily for 3 months. Patients will receive their standard JIA treatment plus placebo. Outcome Measures. Primary Outcome Measures : Disease Activity Evaluation [ Time Frame: 3 months ] Clinical efficacy will be assessed by calculating the Clinical Juvenile Arthritis Disease Activity Score cJADAS at baseline and at the end of the 3-month trial period.

Secondary Outcome Measures : Serum Malondialdehyde [ Time Frame: 3 months ] an oxidative stress markers, Malondialdehyde MDA will be assessed form patients sera at baseline and after 3 months. It will be measured using ELISA Kits. serum samples will be withdrawn from each patient at baseline and after 3 months.

About Mito. As the autiommune are responsible for producing energy, any autooimmune that has an Coenzyme Q and autoimmune diseases problem could be related to the Coenzyme Q and autoimmune diseases. Over 50 million people in the U. suffer from these chronic degenerative disorders. While it cannot yet be said that mitochondrial defects cause these problems, it is clear that mitochondria are involved because their function is measurably disturbed. Even autoimmune diseases such as multiple sclerosis, Sjogrens syndrome, lupus, and rheumatoid arthritis appear to have a mitochondrial basis to illness.

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