Kendal Broadie
Faculty Member
Last active: 5/27/2014

Matrix metalloproteinases and minocycline: therapeutic avenues for fragile X syndrome.

Siller SS, Broadie K
Neural Plast. 2012 2012: 124548

PMID: 22685676 · PMCID: PMC3364018 · DOI:10.1155/2012/124548

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.

MeSH Terms (10)

Animals Disease Models, Animal Drosophila Fragile X Syndrome Humans Matrix Metalloproteinase Inhibitors Matrix Metalloproteinases Mice Minocycline Protease Inhibitors

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