and clinical trials
Idebenone studies in regards to therapy of Alzheimer's disease have been inconsistent, but there may be a trend for a slight benefit.
May benefit those with Friedreich's ataxia. See studies below.
Has not been found to be helpful in Huntington's disease.
Idebenone side effects, safety
The most common side effects associated with idebenone are insomnia, stomach pain, nausea, and anxiety.
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Idebenone may be helpful in Friedreich's ataxia
Clinical experience with high-dose idebenone in
J Neurol. 2009; Schulz JB, Di Prospero NA, Fischbeck K. Department of Neurology, University Medical Centre, RWTH Aachen, Pauwelsstr. 30, 52074, Aachen, Germany.
Several reports in the literature describe the effects of low-dose (5 mg/kg/day) idebenone in significantly reducing cardiac hypertrophy in patients with Friedreich ataxia. However, the effects of idebenone on neurological function have not been reliably determined in these studies; when neurological parameters were reported, results were often inconclusive, usually because of subject heterogeneity and lack of adequate statistical power. In two of these studies, some patients showed beneficial effects of idebenone on their cardiomyopathy only when the dose was increased, prompting the systematic investigation of higher doses of idebenone. Following a phase 1 dose escalation study, a phase 2 tolerability and efficacy trial with low, intermediate, and high doses of idebenone was conducted. The results suggested that treatment with intermediate- and high-dose idebenone had beneficial effects on neurological symptoms. On the basis of these results, two phase 3 trials have been initiated, one in the United States with young ambulatory patients and one in Europe without limits on age and disease severity.
Neurological effects of high-dose
idebenone in patients with Friedreich's
ataxia: a randomised, placebo-controlled
Lancet Neurol. 2007. Di Prospero NA, Baker A, Jeffries N, Fischbeck KH. Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. Friedreich's ataxia is a progressive, multisystem, degenerative disorder caused by a reduction in frataxin. Loss of frataxin results in mitochondrial dysfunction and oxidative damage in patients and model systems. Previous studies have indicated that the antioxidant idebenone (5 mg/kg daily) reduces cardiac hypertrophy, but definite improvement in neurological function has not been shown. 48 genetically confirmed Friedreich's ataxia patients, aged 9-17 years, were enrolled in a 6-month, randomised, double-blind, placebo-controlled study. The patients received placebo or one of three doses of idebenone (approximately 5 mg/kg, 15 mg/kg, and 45 mg/kg), stratified by body weight. Treatment with higher doses of idebenone was generally well tolerated and associated with improvement in neurological function and ADL in patients with Friedreich's ataxia. The degree of improvement correlated with the dose of idebenone, suggesting that higher doses may be necessary to have a beneficial effect on neurological function.
Cerebrospinal fluid concentrations of idebenone in Friedreich ataxia
We studied plasma and cerebrospinal fluid (CSF) concentrations of idebenone in five Friedreich ataxia patients on treatment with this antioxidant, and plasma and CSF ubiquinone-10 (Q (10)) concentrations in 15 controls. CSF idebenone concentrations were below the detection limit in 3 Friedreich ataxia patients and no association could be demonstrated between plasma and CSF idebenone values. Q (10) CSF concentrations were approximately 300 times lower than those of plasma. No correlation was observed between plasma and CSF Q (10) concentrations. A significantly positive correlation was observed between CSF total protein values and CSF Q (10) concentrations . Our findings suggest that less idebenone is distributed to the brain than to other tissues, although CSF does not appear to be an appropriate material for treatment monitoring of idebenone and other quinoid compounds.
Idebenone delays the onset of cardiac functional alteration without
correction of Fe-S enzymes deficit in a mouse model for Friedreich ataxia.
Hum Mol Genet. 2004.
Friedreich ataxia (FRDA), a progressive neurodegenerative disorder associated with cardiomyopathy, is caused by severely reduced frataxin, a mitochondrial protein involved in Fe-S cluster assembly. We have recently generated mouse models that reproduce important progressive pathological and biochemical features of the human disease. Our frataxin-deficient mouse models initially demonstrate time-dependent intramitochondrial iron accumulation, which occurs after onset of the pathology and after inactivation of the Fe-S dependent enzymes. Here, we report a more detailed pathophysiological characterization of our mouse model with isolated cardiac disease by echocardiographic, biochemical and histological studies and its use for placebo-controlled therapeutic trial with Idebenone. The Fe-S enzyme deficiency occurs at 4 weeks of age, prior to cardiac dilatation and concomitant development of left ventricular hypertrophy, while the mitochondrial iron accumulation occurs at a terminal stage. From 7 weeks onward, Fe-S enzyme activities are strongly decreased and are associated with lower levels of oxidative stress markers, as a consequence of reduced respiratory chain activity. Furthermore, we demonstrate that the antioxidant Idebenone delays the cardiac disease onset, progression and death of frataxin deficient animals by 1 week, but does not correct the Fe-S enzyme deficiency. Our results support the view that frataxin is a necessary, albeit non-essential, component of the Fe-S cluster biogenesis, and indicate that Idebenone acts downstream of the primary Fe-S enzyme deficit. Furthermore, our results demonstrate that Idebenone is cardioprotective even in the context of a complete lack of frataxin, which further supports its utilization for the treatment of FRDA.
Idebenone treatment in Friedreich patients: one-year-long randomized
Neurology. 200. Division of Biochemistry and Genetics, Carlo Besta National Neurological Institute-IRCCS, Milan, Italy.
The authors carried out a 1-year, randomized, placebo-controlled trial of idebenone in 29 patients with Friedreich ataxia. They found significant reductions of interventricular septal thickness and left ventricular mass in the idebenone group vs the placebo group, with no improvement in other heart ultrasound measures or neurologic condition. The absolute cardiac changes were modest, but the findings suggest that larger trials should assess whether idebenone reduces ventricular hypertrophy in patients with Friedreich ataxia.
CNS Drugs. 2014 January. Mitochondrial enhancement for neurodegenerative movement disorders: a systematic review of trials involving creatine, coenzyme q10, idebenone and mitoquinone. Neurodegenerative movement disorders mainly include Parkinson's disease (PD), atypical parkinsonisms, Huntington's disease (HD), and Friedreich's ataxia (FA). With mitochondrial dysfunction observed in these diseases, mitochondrial enhancement such as creatine, coenzyme Q10 (CoQ10) and its analogues (idebenone and mitoquinone) has been regarded as a potential treatment. There is insufficient evidence to support the use of mitochondrial enhancement in patients with neurodegenerative movement disorders. More well-designed RCTs with large samples are required for further confirmation.
Alzheimer's disease and dementia
Idebenone treatment fails to slow cognitive decline in Alzheimer's disease.
To determine the effect of idebenone on the rate of decline in Alzheimer's disease (AD). A 1-year, multicenter, double-blind, placebo-controlled, randomized trial was conducted. Subjects were over age 50 with a diagnosis of probable AD and had Mini-Mental State Examination (MMSE) scores between 12 and 25. Subjects were treated with idebenone 120, 240, or 360 mg tid, each of which was compared with placebo. Primary outcome measures were the Alzheimer's Disease Assessment Scale-Cognitive Subcomponent (ADAS-Cog) and a Clinical Global Impression of Change (CGIC). Secondary outcome measures included measurements of activities of daily living, the Behavioral Pathology in Alzheimer's Disease Rating Scale, and the MMSE. Five hundred thirty-six subjects were enrolled and randomized to the four groups. Except for a slight difference in age, there were no differences in patient characteristics at baseline. For the primary outcome measures, there were no significant overall differences between the treatment groups in the prespecified four-group design. In an exploratory two-group analysis comparing all three treated groups combined with placebo, drug-treated patients performed better on the ADAS-Cog in both the intent-to-treat (ITT) and completers analyses. There were no differences in the CGIC scores for the ITT or completers analyses in either the four-group or the two-group analyses. There were no overall differences on any of the secondary outcome measures in any of the analyses. Idebenone failed to slow cognitive decline in AD that was of sufficient magnitude to be clinically significant.
Use of Noben (idebenone) in the treatment
of dementia and memory impairments without dementia.
Neurosci Behav Physiol. 2009. Voronkova KV, Meleshkov MN. Department of Neurology and Neurosurgery, Russian State Medical University, Moscow, Russia.
Noben (idebenone) at a dose of 120 mg per day for six months was used in the treatment of 35 patients aged 60-86 years with Alzheimer's-type dementia, mixed dementia, and memory impairments not reaching the stage of dementia. Patients were assessed on the basis of data from somatic, neurological, and psychiatric investigations, as well as neuropsychological testing and a series of psychometric and other scales and tests, before and after treatment. Significant improvements in patients' conditions on the MMSE were seen in patients with mild and moderate dementia. Improvements in daily activities were obtained in 27% of patients. Neuropsychological investigations demonstrated improvements in short-term and long-term memory and attention, with improvements in speech functions, performance of kinesthetic, spatial, and dynamic praxis tests, and in visuospatial gnosis, thought, and writing. On the CGI scale, positive treatment effects were obtained in 37% of patients, while 48% of patients remained in a stable state.
Idebenone as antioxidant
Tolerability and improved protective action of idebenone-loaded pegylated liposomes on ethanol-induced injury in primary cortical astrocytes.
J Pharm Sci. 2004.
The potential therapeutic advantages of the encapsulation of idebenone within pegylated liposomes were investigated in vitro on primary cortical astrocytes of rats. In particular, both the concentration-dependent effects and the therapeutic effectiveness toward excitotoxic injury, elicited by chronic treatment with ethanol for 12 days, were evaluated. The following parameters were taken into consideration to assay free or liposomally entrapped idebenone: lactic dehydrogenase release, respiratory capacity measured by tetrazolium salt conversion, glutamine synthetase, and the levels of constitutive and inducible 70-kDa heat shock proteins. To evaluate the effects on astrocytes, three different drug concentrations were used. At the highest concentration used (50 microM), a toxic effect of the free and liposomally entrapped drug was observed. Toxic effects seem to be due to a cellular membrane perturbation, as demonstrated by (45)Ca(2+) permeation. The therapeutic effect of free or liposomally entrapped idebenone on ethanol-induced injury of primary cortical astrocytes was evaluated as a function of the drug concentration. The drug liposome formulation was much more effective than the free drug in counteracting the ethanol-induced damage in astrocytes, i.e., 10-times-lower doses of liposomally entrapped idebenone are able to provide a greater protective action than the free drug. The improved action of idebenone-loaded liposomes is probably due to the greater drug bioavailability at the cellular level.
Quinone analogues regulate mitochondrial substrate competitive oxidation.
Biochem Biophys Res Commun. 2004.
Quinone derivatives are among the rare compounds successfully used as therapeutic reagents to fight mitochondrial diseases. The effect of four quinone derivatives was comparatively studied on NADH- and succinate-competitive oxidation by a sub-mitochondrial fraction. Under our experimental conditions, the less hydrophobic derivatives (menadione, duroquinone) poorly affected electron flow from either NADH or succinate to oxygen, yet readily diverting electrons from isolated complex I. This latter effect was abolished by succinate addition. More hydrophobic derivatives (idebenone, decylubiquinone) stimulated oxygen uptake from succinate. But while NADH oxidation was slightly inhibited by idebenone, it was somewhat increased by decylubiquinone. As a result, idebenone strongly favoured succinate over NADH oxidation. This study therefore suggests that any therapeutic use of quinone analogues should take into account their specific effect on each respiratory chain dehydrogenase.
Q. My son was diagnosed with LHON in July 2006 after going blind in his right eye on May 17th. I had read about a study in England, and asked them the amount of idebenone they were prescribing for it. I then had my son take the 900mg which he started in Aug. He is also on Low dose Naltroxone 4.5mg which he has been on for a year, and to help him even more he is also on 600mg of COQ10. It has been over year since he was first affected, and the doctors at Bascom Palmer in Miami, FL. are very surprised since he has the worst case scenario of the illness being 117 78 A>G and homoplastic. They have never seen anyone go for more than eight months without it affecting both eyes. I was wondering if there were any long term side affects that he might develop? Is there any studies being done with these combination of drugs?
A. We are not aware of any studies with these supplements for this condition. LHON or Leber's Hereditary Optic Neuropathy is a rare condition which can cause loss of central vision.
Q. Your book Mind Boosters, which I have just purchased,
is full of useful info, especially the reports of personal experiences. I am interested in
Alzheimer's Disease. One substance not specifically mentioned in the book is the synthetic
form of CoQ10, "Idebenone", which is claimed to work better than CoQ10, and
especially in AD. It works as an antioxidant, brain metabolism enhancer (like CoQ10) but
is said also to regulate neurotransmitters like serotonin, stimulate production of Nerve
Growth Factor, and protect against glutamate/aspartate nerve damage. Long-term trials with
it in AD in Japan have apparently had very good results. I would be very interested to
hear if you have any opinions/comments or personal experiences concerning Idebenone,
either in general or specifically concerning AD.
A. I was planning to include idebenone and other less known nutrients in my book, but then I decided to limit them since it would have been too thick a book and too complicated and detailed for the mainstream consumer. There is some good research with idebenone but it will take a long time to find out more about it and its practical uses. I have not used it clinically so I don't have any first hand experience.
Q. Can you tell me about idebenone cream?
A. I am not familiar with idebenone cream.
Q. Is it supposed to have better or wider effects than CoQ10.
A. I have not seen any comparison studies between idebenone and Coenzyme Q10 to determine which one is better to take as a supplement. For the time being, it is preferable to stay with regular CoQ10 since it has been studied quite extensively.
I am a 43 year old woman with LHON eye disease.
I lost my sight at 23 and am now legally blind. I have 3 children ages 12, 10
and 3 who are also at risk . We have the 3460 mutation, We have 7 people in our
family with vision loss. I now give my children liquid Co Q 10 but want to know
if idebenone would be good for a preventative for children or is it only useful
in the acute phase of vision loss. I feel very alone in this struggle to help my
young children not go blind.
Leber Hereditary Optic Neuropathy (LHON) was first described in 1871. It involves a sudden loss of vision in young men with a family history of blindness. LHON is a maternally inherited disorder characterized by bilateral, often sequential vision loss, before and during progressive visual deterioration. Unfortunately we are not familiar with the treatment of this condition.
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