Progress and Prospects in Parkinson's Research/Therapy/Neuroprotection/Co-Enzyme Q10

Background
Co-Enzyme Q10 is also known as ubiquinone, ubidecarenone, coenzyme Q and CoQ10 and is found in all eukaryotic cells, where it forms a key component of the metabolism of oxygen into Adenisone TriPhosphate (ATP) by mitochondria.

Research
1999

Schults et al found that oral CoQ10 protected the nigrostriatal dopaminergic system in one-year-old mice treated with MPTP.

2002

Schults et al took 80 subjects with early PD who did not require treatment for their disability and made a random assignment to placebo or coenzyme Q10 at dosages of 300, 600, or 1200 mg/d.

The progress of their PD was measured over 16 months. The adjusted mean total UPDRS changes were +11.99 for the placebo group, +8.81 for the 300-mg/d group, +10.82 for the 600-mg/d group, and +6.69 for the 1200-mg/d group. The conclusion was that the administration of CoQ10lows down the progresssion of PD.

2003

Schults  reviewed the evidence that CoQ10 can slow the functional decline in PD.

2004

Schults et al assessed the optimum level of CoQ10 that could be tolerated. They gave increasing doses to 17 patients together with a stable dosage of Vitamin E (apha-tocopherol). and measured the corresponding levels in serum.

The results suggested that a dosage of 2400 mg/day (with vitamin E/alpha-tocopherol 1200 IU/day) is an appropriate highest dosage to be studied.

2007

Galpern and Cudkowicz make the case for treating neurodegenerative diseases including amyotrophic lateral sclerosis, Huntington's disease, and Parkinson's disease with CoQ10, which is safe and well tolerated.

2008

Cleren et al established a number of benefits of CoQ10 in animal models.

1.	Administration in the diet resulted in significant protection against loss of dopamine (DA), which was accompanied by a marked increase in plasma concentrations of CoQ10.

2.	Neuroprotection was stablished against MPTP -induced loss of DA using both CoQ10, and reduced CoQ10.

3.	They found neuroprotective effects against DA depletion, loss of tyrosine hydroxylase neurons and induction of alpha-synuclein inclusions in the substantia nigra pars compacta.

2009

Faust et al reported on a series of experiments on fruit flies:-

"In the present study, a Drosophila DJ-1A model of PD was used to test potential neuroprotective drugs. The drugs applied are the Chinese herb celastrol, the antibiotic minocycline, the bioenergetic amine coenzyme Q10 (coQ10), and the glutamate antagonist 2,3-dihydroxy-6-nitro-7-sulphamoylbenzo[f]-quinoxaline (NBQX). All of these drugs target pathogenic processes implicated in PD, thus constitute mechanism-based treatment strategies. We show that celastrol and minocycline, both having antioxidant and anti-inflammatory properties, confer potent dopaminergic neuroprotection in Drosophila DJ-1A model, while coQ10 shows no protective effect. NBQX exerts differential effects on cell survival and brain dopamine content: it protects against DN loss but fails to restore brain dopamine level."