Critical data‐based re‐evaluation of minocycline as a putative specific microglia inhibitor
Thomas Möller(University of Washington), Frédérique Bard(Janssen (United States)), Anindya Bhattacharya(Janssen (United States)), Knut Biber(University Medical Center Groningen), Brian Campbell(Lundbeck (United States)), Elena Dale(Lundbeck (United States)), Claudia Eder(St George's, University of London), Li Gan(Gladstone Institutes), Gwenn A. Garden(University of Washington), Zoë A. Hughes(Pfizer (United States)), Damien D. Pearse(University of Miami), Roland G. W. Staal(Lundbeck (United States)), Faten A. Sayed(Gladstone Institutes), Paul D. Wes(Lundbeck (United States)), Hendrikus Boddeke(University Medical Center Groningen)
Cited by 195
Abstract
Minocycline, a second generation broad-spectrum antibiotic, has been frequently postulated to be a "microglia inhibitor." A considerable number of publications have used minocycline as a tool and concluded, after achieving a pharmacological effect, that the effect must be due to "inhibition" of microglia. It is, however, unclear how this "inhibition" is achieved at the molecular and cellular levels. Here, we weigh the evidence whether minocycline is indeed a bona fide microglia inhibitor and discuss how data generated with minocycline should be interpreted. GLIA 2016;64:1788-1794.
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