Landmark 171 · Trial in people
MitoQ (PROTECT)
No difference from placebo in 128 newly diagnosed people over 12 months. It did not slow Parkinson's.
In short
A pill designed to sit inside mitochondria and mop up damaging oxygen molecules did nothing to slow progression in 128 newly diagnosed people over 12 months.
- What it is
- Trial in people
- Outcome
- Did not work
- When
- 2010
- Size
- 128 people · Phase 2
- Approach
- Help cells clean up
- Research lane
- Mitochondria & energy
- Trial registry
- NCT00329056
- Last checked
- 19 Oct 2026
The research record
This is the project's file for this landmark, as written and checked. Sources are listed at the end; anything not yet confirmed is marked "Not yet verified".
Who
B. J. Snow and colleagues (the Otago repository holds the record, so the work is linked to New Zealand). Sponsor: Antipodean Pharmaceuticals. The drug, mitoquinone (MitoQ), is a form of coenzyme Q10 chemically tied to a carrier that makes it collect inside mitochondria. Published in Movement Disorders 2010;25:1670–1674. The registry gives May 2006 to November 2007 for the trial itself.
What happened
Mitochondria are the cell's power plants, and they make harmful oxygen by-products. Parkinson's brains show a fault in the first step of the energy chain (landmark 11). MitoQ was meant to protect mitochondria from that damage better than ordinary antioxidants.
- Design. Double-blind, placebo-controlled. 128 newly diagnosed, untreated people took one of two MitoQ doses (40 mg or 80 mg once daily, per the registry) or placebo for 12 months. Main measure: change in the total UPDRS score (a standard symptom rating scale).
- Result. No difference between MitoQ and placebo on any measure of progression. The authors concluded that MitoQ does not slow Parkinson's and that this should be weighed against the oxidative-stress idea of the disease.
Why it moved us toward a cure
It was a direct test of a specific version of the mitochondrial idea: that mopping up oxygen damage inside mitochondria would slow the disease. The answer was no. It sits beside the energy-supplement failures, and pushed the field toward fixing mitochondrial quality control instead (see landmark 11 for the starting observation).
Outcome
Dead end for mitochondria-targeted antioxidants as a slowing treatment. The mitochondria branch continues through other approaches.
Sources
- Snow et al., Mov Disord 2010; abstract via Europe PMC (PMID 20568096) · DOI 10.1002/mds.23148 · Otago repository record
- ClinicalTrials.gov NCT00329056
- Not yet verified: the exact effect sizes and per-arm numbers (only the abstract was read); the doses are from the registry, not the paper. The registry says Phase 2.
How it connects
Built on
- tests Complex I deficiency in the Parkinson's brain · 1989
Led to
None recorded.