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To the Editor:
We read with interest the Special Article by Ravina et al. proposing neuroprotective candidate drugs for clinical trials in Parkinson’s disease (PD).1 Minocycline, which has already been launched for phase II/III trials in PD, Huntington’s disease (HD), and atypical parkinsonism, is one of the 21 selected drugs that passed a set of predefined evaluation criteria: primary mechanism(s), consistency of preclinical data, blood-brain barrier penetration, safety/tolerability ratio, and relevant animal model efficacy. The pharmacokinetics and mechanisms of anti-inflammatory/antiapoptotic actions of minocycline are well known.1 There is some evidence that minocycline might confer neuroprotection in rodent models of PD-like neurodegeneration and transgenic model of HD, using various doses and routes of administration.1,2⇓
In contrast with those latter, our own experiments fail to show beneficial effects of minocycline in three different animal models (unpublished data). Using a progressive 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) nonhuman primate model that replicates the progressive nature of PD,3 we observed that minocycline (200 mg twice daily, 12 hours apart, minocycline generic) treatment had a deleterious effect. Indeed, while MPTP-placebo-treated animals displayed mild parkinsonism at day 15 (mean motor score = 5 ± 0.6), the minocycline/MPTP-treated tended to be more affected (11 ± 1.2, p = 0.057, Mann-Whitney), suggesting that minocycline/MPTP-treated animals developed symptoms more rapidly and severely.
Striatal sections from both groups were processed at day 15 for dopamine transporter binding,2 compared to control animals. The minocycline/MPTP-placebo-treated animals showed …
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