Minocycline does not affect amyloid β phagocytosis by human microglial cells

Activated microglia accumulate in amyloid β (Aβ) plaques containing amyloid associated factors SAP and C1q in Alzheimer's disease (AD) brain. Microglia are involved in AD pathogenesis by promoting Aβ plaque formation and production of pro-inflammatory cytokines. On the other hand, phagocytosis of Aβ by activated microglia may prevent Aβ-mediated neurotoxicity and Aβ 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-α by human microglia upon exposure to a mixture of Aβ, 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 β fibrils.