Journal of Psychopharmacology 17(4) (2003) 461 2003 British Association for Psychopharmacology (ISSN 0269-8811) Letter to the Editors
Why minocycline is helpful in Huntington’s disease Raphael M. Bonelli and Hans-Peter Kapfhammer University Clinic of Psychiatry, Karl-Franzens University Graz, Austria.
We would like to congratulate Denovan-Wright and colleagues for brain able to restore function even with the toxic pathways being their important observation (Denovan-Wright et al., 2002) in a blocked? The recent findings may lead in this direction.
recent issue of the Journal of Psychopharmacology. They treated a Ona et al. (1999) and Chen et al. (2000) started minocycline ‘in patient with advanced Huntington’s disease (HD) with minocycline the late presymptomatic stage’ of transgenic HD mice. It would be for more than 1 year and observed positive effects. They suggest interesting to repeat their trials in a symptomatic stage to that minocycline may be of benefit in those patients with advanced investigate a possible duplication of the effects observed by HD and can be used safely in these patients.
Yamamoto et al. (2000), which would be clinically more relevant.
We ourselves found a similar improvement of motor function in A double-blind, placebo-controlled trial appears highly warranted 10 out of 14 patients and an amelioration of cognitive function in to definitively establish the value of minocycline in HD.
seven out of 14 HD patients with minocycline after 6 months onthe drug (Bonelli et al., 2003) and underline their conclusions. Weobserved these ameliorative effects in all HD stages, not only in the advanced group, as suggested by Denovan-Wright and colleagues,and so would extend their suggestion to all symptomatic HD patients. Ona et al. (1999) previously demonstrated evidence of University Clinic of PsychiatryKarl-Franzens University Graz caspase-1 activation in the brains of R6/2 transgenic mouse models mice and humans with the disease. In the mouse model, expression of a dominant-negative caspase-1 mutant extended survival and E-mail: [email protected] delayed the appearance of neuronal inclusions, neurotransmitterreceptor alterations and onset of symptoms, indicating thatcaspase-1 is important in the pathogenesis of HD. The authors also demonstrated that intracerebroventricular administration of acaspase inhibitor delayed disease progression and mortality in the Alarcon G S (1998) Minocycline for the treatment of rheumatoid arthritis. Rheum Dis Clin North Am 24: 489–499 mouse model. (Ona et al., 1999).
Berger A (2000) Minocycline slows progress of Huntington’s disease Subsequently, Chen et al. (2000) decided to evaluated the therapeutic efficacy of minocycline in mouse model of HD after Bonelli R M, Heuberger C, Reisecker F (2003) Minocycline for Huntington’s disease: an open label study. Neurology 60:883–884 Yrjanheikki et al. showed that mice treated with minocycline both Chen M, Ona V O, Li M, Ferrante R J, Fink K B, Zhu S, Bian J, Guo before and after the induction of stroke seemed to sustain less brain L, Farrell L A, Hersch S M, Hobbs W, Vonsattel J P, Cha J H, damage (Berger, 2000). Minocycline delayed disease progression, Friedlander R M (2000) Minocycline inhibits caspase-1 andcaspase-3 expression and delays mortality in a transgenic inhibited caspase-1 and caspase-3 mRNA upregulation, and mouse model of Huntington disease. Nature Med 6: 797–801 decreased inducible nitric oxide synthetase activity in the R6/2 Denovan-Wright E M, Devarajan S, Dursun S M, Robertson H A model. Survival was extended by 14%. Effective pharmacotherapy (2002) Maintained improvement with minocycline of a patientwith advanced Huntington’s disease. J Psychopharmacol 16: in R6/2 mice required caspase-1 and caspase-3 inhibition. (Chen et Langevitz P, Livneh A, Bank I, Pras M (2000) Benefits and risks of Minocycline is a second-generation tetracycline commonly minocycline in rheumatoid arthritis. Drug Saf 22: 405–414 used for a prolonged period to treat acne and rheumatoid arthritis.
Ona V O, Li M, Vonsattel J P, Andrews L J, Khan S Q, Chung W M, Frey A S, Menon A S, Li X J, Stieg P E, Yuan J, Penney J B, (Alarcon, 1998; Patel et al., 1998; Langevitz et al., 2000) It Young A B, Cha J H, Friedlander R M (1999) Inhibition of effectively crosses the blood-brain barrier and inhibits IL-1β- caspase-1 slows disease progression in a mouse model ofHuntington’s disease. Nature 399: 263–267 converting enzyme and inducible nitric oxide synthase up- Patel K, Cheshire D, Vance A (1998) Oral and systemic effects of regulation in animal models of ischemic stroke. After ischemia, prolonged minocycline therapy. Br Dent J 185: 560–562 minocycline inhibits caspase-1 and inducible nitric oxide Tikka T M, Koistinaho J E (2001) Minocycline provides synthetase upregulation, and reduces infarction (Chen et al., 2000).
neuroprotection against n-methyl-d-aspartate neurotoxicity byinhibiting microglia. J Immunol 166: 7527–7533 Minocycline protects neurons in mixed spinal cord cultures against Yamamoto A, Lucas J J, Hen R (2000) Reversal of neuropathology NMDA excitotoxicity (Tikka and Koistinaho, 2001).
and motor dysfunction in a conditional model of Huntington’s What is the explanation for the findings of Denovan-Wright and Yrjanheikki J, Tikka T, Keinanen R, Goldsteins G, Chan PH, our group? The disappearance of aggregates and symptoms in the Koistinaho J (1999) A tetracycline derivative, minocycline, HD mice studied by Yamamoto et al. (2000) (i.e. by switching on reduces inflammation and protects against focal cerebral or off the mutant exon 1 HD gene) suggests that mutant proteins ischemia with a wide therapeutic window. Proc NatlAcad Sci U S A 96:13496-13500 can be cleared even after the cells manifest dysfunction. Is the

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