Minocycline does not affect amyloid beta phagocytosis by human microglial cells

Atoosa Familian, Piet Eikelenboom, Robert Veerhuis

Research output: Contribution to JournalArticleAcademicpeer-review

43 Citations (Scopus)


Activated microglia accumulate in amyloid beta (Abeta) plaques containing amyloid associated factors SAP and C1q in Alzheimer's disease (AD) brain. Microglia are involved in AD pathogenesis by promoting Abeta plaque formation and production of pro-inflammatory cytokines. On the other hand, phagocytosis of Abeta by activated microglia may prevent Abeta-mediated neurotoxicity and Abeta plaque formation. Minocycline, a tetracycline derivative, is neuroprotective in various neurodegenerative models as well as human chronic neurological disorders. Minocycline attenuates the release of TNF-alpha by human microglia upon exposure to a mixture of Abeta, SAP and C1q. Here, we demonstrate that minocycline down-regulates the production of pro-inflammatory cytokines by human microglia without affecting their beneficial activity, phagocytosis of amyloid beta fibrils
Original languageEnglish
Pages (from-to)87-91
JournalNeuroscience letters
Issue number1
Publication statusPublished - 2007

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