Elsevier

Neuroscience Letters

Volume 416, Issue 1, 6 April 2007, Pages 87-91
Neuroscience Letters

Minocycline does not affect amyloid β phagocytosis by human microglial cells

https://doi.org/10.1016/j.neulet.2007.01.052Get rights and content

Abstract

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.

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Acknowledgements

We thank the Netherlands Brain Bank (coordinator Dr. R. Ravid) for supplying the human CNS tissue, and Mrs. M Jacobs for technical assistance.

This study was supported by grants from Alzheimer Nederland (V-2000-008) and from the Internationale Stichting Alzheimer Onderzoek (ISAO grant: 03509) and stichting Dioraphte.

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