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Updated: Jul 16, 2026

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia
Published on: November 9, 2018
Minocycline does not affect amyloid beta phagocytosis by human microglial cells
Atoosa Familian1, Piet Eikelenboom, Robert Veerhuis
1Department of Psychiatry, VU University Medical Center, Amsterdam, The Netherlands. a.familian@vumc.nl
Abstract:
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.
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