Minocycline does not affect amyloid β phagocytosis by human microglial cells

Activated microglia accumulate in amyloid 3 (A beta) plaques containing amyloid associated factors SAP and C1q in Alzheimer's disease (AD) brain. Microglia are involved in AD pathogenesis by promoting A beta plaque formation and production of pro-inflammatory cytokines. On the other hand, phagocytosis of A beta by activated microglia may prevent A beta-mediated neurotoxicity and A beta 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 A beta, 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. (c) 2007 Elsevier Ireland Ltd. All rights reserved.