CoQ10 is used both topically and internally for the treatment of chronic periodontal disease. Topical application has been shown to improve adult peridontitis (Hanioka et al 1994) and a small open study has shown that oral CoQ10 supplementation can produce dramatic results within 5-7 days, making location of baseline biopsy sites impossible (Wilkinson et al 1975).
There is currently much speculation about the aetiology of Parkinson's disease. Recent experiments suggest that mitochondrial impairment may play a role in the degeneration of nigrostriatal dopaminergic neurons (Ebadi et al 2001, Gotz et al 2000). Additionally, oxidative damage and inflammation are now considered contributing factors.
A number of preclinical studies using in vitro and in vivo models of Parkinson's disease have demonstrated that CoQ10 can protect the nigrostriatal dopaminergic system, and levels of CoQ10 have been reported to be decreased in blood and platelet mitochondria from subjects with Parkinson's disease (Shults 2005). As a result, a multicentre study was conducted to determine whether CoQ10 supplementation would exert beneficial effects in the disease.
The randomised, placebo-controlled double-blind study compared three different doses of CoQ10 (300 mg, 600 mg or 1200 mg) with placebo in 80 subjects with early Coenzyme Q10 306
Parkinson's disease. After 9 months of treatment, subjects taking 1200 mg CoQ10 © 2007 Elsevier Australia
daily experienced significant improvements in disability compared with the placebo group. CoQ10 was also well tolerated at the dosages studied (Shults et al 2002). In 2003, results were published of a double-blind placebo controlled study that showed that even a relatively low dose CoQ10 (360 mg/day) taken for a short period (4 weeks) produced a significant mild benefit on Parkinson's disease symptoms and significantly improved visual function compared with placebo (Muller et al 2003).
The safety and tolerability of high dose CoQ10 in subjects with Parkinson's disease was investigated in an open study of 17 patients (Shults et al 2004). The study used an escalating dosage of 1200, 1800, 2400, and 3000 mg/day administered together with vitamin E (alpha-tocopherol) 1200 lU/day and failed to identify any serious adverse effects with CoQ10 administration. It also identified that plasma CoQ10 levels reached a plateau at 2400 mg/day, suggesting that higher treatment doses are not required.
Similarly to Parkinson's disease, mitochondrial dysfunction and oxidative damage appear to play a role in the pathogenesis of Alzheimer's dementia and therefore CoQ10 supplementation has been investigated as a possible treatment. Currently, evidence is limited to test tube and animal studies and is far from definitive.
Recently, CoQ10 was shown to inhibit beta amyloid formation in vitro (Ono et al 2005) and protect against brain mitochondrial dysfunction induced by a neurotoxic beta-peptide in a study using brain mitochondria isolated from diabetic rats (Moreira et al 2005). McDonald et al (2005) conducted two studies with test animals and found that supplemental CoQ10 (123 mg/kg/day) taken with alpha-tocopherol acetate (200 mg/kg/day) improved age related learning deficits; however, supplementation of CoQ10 alone at this dose, or higher doses of 250 or 500 mg/kg/day, failed to produce comparable effects.
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