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Co-Q 10 Information Summary

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A number of compounds were identified as candidates for further study by the Committee to Identify Neuroprotective Agents in Parkinson's (CINAPS). Of these compounds, Minocycline, Creatine , CoQ10 and GPI 1485 have been selected for testing in the Neuroprotection Clinical Trial.

CO-Q 10

This popular 'health supplement' is a mitochondrial enzyme with antioxidant properties, which can potentially limit oxidative damage in PD. Early untreated PD patients were found to have reduced CoQ10 levels in platelets, lending further support for consideration of this mitochondrial enzyme as a therapeutic target. This drug appears to be well tolerated with few side effects in PD patients at doses less than 800 mg/day. However, no change in Unified Parkinson's Disease Rating Scale (UPDRS) scores was observed at these doses.

Scientific Rationale

  • Complex 1 mitochondrial activity is reduced in Substantia Nigra in post-mortem studies in PD and in the platelets of early, untreated PD patients.
  • Complex 1 is susceptible to oxidative damage.
  • CoQ 10 is an essential component of Complex 1 and II in humans. It serves as an electron acceptor and antioxidant that can potentially limit oxidative damage to complex I.
  • CoQ 10 levels were reduced in platelet mitochondria in early untreated PD patients.
S chapira, J Neurochem 1990; 54:823-827
Haas et al. Ann Neurol. 1995;37:714-722
Jha, J Biol Chem 2000;275:26096-26101
Schulz, Exp Neurol 1995; 132: 279-283 [abstract]
Shults et al. Ann Neurol. 1997;42:261-264 [abstract]

Animal Model Data

RODENT

Mice: chronic intoxication with MPTP with 400 mg/kg CoQ x 10 days before MPTP treatment. CoQ + nicotinamide completely prevented DA depletion (not CoQ alone)

Aged Mice: CoQ10 (oral) 200 mg/kg/day x 5 wks attenuated the decrease in striatal DA concentrations caused by MPTP

S chulz, Exp Neurol 1995; 132: 279-283
Beal, Brain Res 1998;783:109-114

Pharmacokinetics (including blood brain barrier (BBB) penetration)

In animals, oral administration resulted in a significant effect on striatal DA, and therefore likely crosses the BBB. Oral supplemental with CoQ increased brain mitochondrial levels

S chulz, Exp Neurol 1995; 132: 279-283
Matthews et al. PNAS 1998;95:8892-8897.

Safety/Tolerability in Humans

In an open label, pilot study of 10 PD patients, CoQ 10 at 200 mg/day for 3 months was administered. There were no changes in UPDRS and no side effects were reported. 15 PD patients were given one of 3 oral doses of Co Q10 in a Vit E vehicle (400, 600 or 800 mg/day) x one month. All doses were associated with significantly increased CoQ10 levels in plasma and there were no side effects and it was well tolerated. At 800 mg/day, there were increased casts in urine in 2/5 patients. No change in UPDRS, but patients were on PD meds.

S trijks, Molec Aspects Med, 1997;18(suppl): S237-S240
Shults, Neurology 1998; 50:793-795

Drug Interaction Potential

P atients in the Shults '98 study (above) were all receiving PD meds, no interactions were detected.

Clinical Trial/Epidemiological Evidence in Human PD

In The CARE HD trial, patients with HD tolerated 600mg/day of CoQ-10 well and showed a trend in functional improvement that was not statistically significant. In the QE2 study: 80 de novo PD subjects on placebo, 300, 600, 1200mg day of CoQ followed until need for symptomatic therapy, up to 16 months. UPDRS change was primary outcome measure. Test for linear trend between groups on UPDRS( primary analysis) negative but difference in rate of change between 1200mg group (7pts) and placebo (12pts).

H SG, Neurology 2001 57: 397-404
Shults, Arch Neurol. 2002 Oct;59(10):1541-1550.

Last updated July 01, 2008