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Neural Plasticity
Volume 2012, Article ID 124548, 9 pages
Review Article

Matrix Metalloproteinases and Minocycline: Therapeutic Avenues for Fragile X Syndrome

1Departments of Biological Sciences and Cell and Developmental Biology, Kennedy Center for Research on Human Development, Vanderbilt University Station B, Nashville, TN 37232, USA
2Stony Brook School of Medicine, Stony Brook University, Stony Brook, NY 11794, USA

Received 29 November 2011; Accepted 24 February 2012

Academic Editor: Laurie Doering

Copyright © 2012 Saul S. Siller and Kendal Broadie. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Fragile X syndrome (FXS) is the most common known genetic form of intellectual disability and autism spectrum disorders. FXS patients suffer a broad range of other neurological symptoms, including hyperactivity, disrupted circadian activity cycles, obsessive-compulsive behavior, and childhood seizures. The high incidence and devastating effects of this disease state make finding effective pharmacological treatments imperative. Recently, reports in both mouse and Drosophila FXS disease models have indicated that the tetracycline derivative minocycline may hold great therapeutic promise for FXS patients. Both models strongly suggest that minocycline acts on the FXS disease state via inhibition of matrix metalloproteinases (MMPs), a class of zinc-dependent extracellular proteases important in tissue remodeling and cell-cell signaling. Recent FXS clinical trials indicate that minocycline may be effective in treating human patients. In this paper, we summarize the recent studies in Drosophila and mouse FXS disease models and human FXS patients, which indicate that minocycline may be an effective FXS therapeutic treatment, and discuss the data forming the basis for the proposed minocycline mechanism of action as an MMP inhibitor.