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08-02-2017

Idebenone, a CoQ10 analogue and mitochondria protector

mitochondria Idebenone is an analogue of coenzyme Q10, an antioxidant vital for cell membranes and an essential component in the mitochondrial transport chain of ATP-producing electrons.
Idebenone is a powerful antioxidant that works under hypoxic (low oxygen) conditions. Because of its ability to inhibit lipid peroxidation, it protects cell membranes and mitochondria from oxidative damage. Idebenone’s antioxidant properties in the central nervous system protect against cerebral ischaemia and nerve damage.

Idebenone also interacts with the electron transport chain and maintains ATP production in ischaemic situations. It has also been shown to stimulate nerve cell growth factor, a characteristic which may be important in the treatment of Alzheimer’s disease and other neurodegenerative disorders.

Slows down ageing

Mitochondria are crucial to maintaining life because they produce over 90% of ATP bioenergy. However, they use huge amounts of oxygen and are thus particularly vulnerable to free radicals, becoming increasingly damaged over time, and as a result, ineffective. The mitochondria most at risk from free radical-induced ageing are those in the heart, brain and skeletal muscle. Mitochondria are also the sites in the body with the highest concentrations of CoQ10 or idebenone.
Unlike CoQ10, idebenone, even in conditions of low oxygen supply that can occur periodically over a lifetime, is a potent scavenger of mitochondrial free radicals, reducing the increasingly significant damage to DNA that occurs with advancing age. Idebenone works even more effectively than CoQ10 within the electron transport chain, maintaining high energy production, even under hypoxic conditions. This is particularly important for heart and brain cells that may be rapidly damaged when ATP production is compromised as a result of poor tissue oxygenation.

Idebenone and cognitive stimulation

A large number of studies examining animal or human brain cells have shown idebenone’s ability to stimulate brain structure and function. Animal and human studies suggest it can stimulate serotonin production even in far from ideal conditions such as in the case of a very low tryptophan diet or in patients with cerebrovascular dementia. Idebenone was shown to boost cholinergic nerve function and learning ability even under hypoxic conditions or when an anti-cholinergic drug was administered.

It increases production of cellular catecholamines (dopamine, adrenalin and noradrenalin) by stimulating cellular uptake of the precursor, amino acid tyrosine. Idebenone restores glucose utilisation (brain fuel) and ATP production in ischaemic rat brains.
In a study of 75 hospitalised males and females suffering from mild to moderate cognitive problems, in which some were given a daily supplement of 90 or 180mg of idebenone, there was an improvement in cognitive performance and general behaviour in the supplemented patients. 1.

Idebenone and Alzheimer’s disease

2. Nerve cell growth factor plays an important role in the growth, survival and protection of the central nervous system’s cholinergic neurons. In Alzheimer’s disease, cholinergic neurons may become damaged and die. In rats, oral administration of idebenone produces an increase in nerve cell growth factor and improves the activity of acetyltransferase-choline 2. 3. In a study on elderly rat brains, idebenone stimulated production of nerve cell growth factor and restored its reduced content. After 21 consecutive days of supplementation, the amount of nerve cell growth factor was back to a level comparable to that of young animals3.
Amyloid-beta peptide, the major constituent of the senile plaques found in Alzheimer’s disease, is neurotoxic, probably via oxidative stress mechanisms. When it is injected intracerebroventricularly into rats, they display significant memory and behaviour problems. However, when the animals are given idebenone and alpha tocopherol before and after the injections, they show no such problems. 4.
In a double-blind, placebo-controlled ,multicentre study, 450 patients received either a placebo for 12 months followed by 90mg of idebenone for a further 12 months three times a day, or 90mg three times a day for 24 months, or 120mg three times a day for 24 months. Significant, dose-dependent improvements were noted in clinical status measures and in neuropsychiatric tests, compared with placebo. These improvements continued throughout the two years of the study5.
A German study tested two doses of idebenone (30mg and 90mg three times a day) on patients with mild to moderate Alzheimer’s disease. In total, 247 patients completed the six-month clinical study. Patients were evaluated using the international Alzheimer’s disease Assessment Scale. On average, patients who took the higher doses of idebenone had a 2.3 improvement on the 120 point scale. The more severe the disease was at the beginning of the study, the more the patients’ condition improved. Those who began the study with a score of at least 20 gained an average 4.1 points compared with placebo. The largest gains were noted in cognitive tasks, patients with the most severe disease and taking the highest doses reaching 6.9 points on the 50 point cognitive scale 6.

Protection against neurotoxicity of amino acid exciters

Glutamic acid and aspartic acid are the two major excitatory amino acid neurotransmitters in the human brain. Without them, we would be in a mentally vegetative state.

Under certain conditions, such as brain trauma or stroke, excessive amounts of excitatory amino acids accumulate in the fluid surrounding brain cells, causing damage and even destroying nerve or glial cells via free radical mechanisms.
The two main dietary sources of excitatory amino acids are monosodium glutamate, a flavour enhancer, and aspartame. In addition, a number of processed foods contain hydrolised vegetable protein, yeast extract, soy protein isolate and similar ingredients that are essentially excitatory amino acids.

In studies on various types of nerve cells and oligodendroglial cells, idebenone demonstrated a powerful protective effect against glutamate toxicity.

Friedrich’s ataxia

In 1999, The Lancet published the results of a study by researchers at INSERM which advocated the use of idebenone in the treatment of this disease. After four to nine months’ administration of idebenone to three young patients with hypertrophic cardiopathy, a significant decrease in cardiac impairment was observed in the three patients. 7. A year-long, double-blind, placebo-controlled study on 29 patients with Friedrich’s ataxia produced a similar result and while the improvements in cardiac impairment were modest, the results point to the need for a larger study to assess whether idebenone could reduce ventricular hypertrophy in patients with this disease8.

Comparing CoQ10 with idebenone

¤ Idebenone is a much more powerful antioxidant than CoQ10. Studies suggest it can actually neutralise free radicals 30 to 100 times more effectively than vitamin E or vinpocetine.

¤ Idebenone is protective even under hypoxic conditions, whereas CoQ10 can actually become pro-oxidant in such circumstances.

¤ Unlike CoQ10, idebenone increases nerve cell growth factor and stimulates cholinergic activity, thus boosting cognitive ability.
¤ Due to its potent antioxidant effect, idebenone protects mitochondria and mitochondrial DNA by sweeping away free radical activity.
1. De Nicola P., Fundamental and clinical assessments of drugs in cerebral circulation and metabolism in vascular dementia, Program and extended abstracts, XIVth World Congress of gerontology, June20, 1989, Acapulco.
2. Nabeshima T. et al., Oral administration of NGF synthesis stimulators recovers reduced brain NGF content in aged rats and cognitive dysfunction in basal-forebrain-lesioned rats, Gerontology, 1994; 40: S46-S56.
3. Nitta A. et al., Oral administration of idebenone, a stimulator of NGF synthesis, recovers reduced NGF content in aged rat brain, Neurosci. Lett., 1993; 163: 219-222.
4. Yamada K. et al., Protective effects of idebedone and alpha-tocopherol on beta-amyloid-(1-42)-induces learning and memory deficits in rats: implication of oxidative stress in beta-amyloid-induced neurotoxicity in vivo, Eur. J. Neurosci., 1999; 11: 83-90.
5. Gutzman H. et al., Sustained efficacy and safety of idebedone in the treatment of Alzheimer's disease: update on a 2-year double-blind multicentre study, J. Neural. Transm., 1998; 54: S301-S310.
6. Weyer G. et al., A controlled study of two doses of idebenone in the treatment of Alzheimer disease, Neuropsychobiology, 1997; 36: 73-82.
7. Rustin P. et al., Effect of idebenone on cardiopathy in Friedreich' ataxia : a preliminary study, Lancet, 1999; 354: 477-479.
8. Mariotti C. et al., Idebenone treatment in friedrich patients : one-year-long randomized placebo-controlled trial, Neurology, 2003; 60: 1676-1679.
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Idebenone 45 mg

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