Fragile X syndrome (FXS) causes behavioural symptoms including hyperactivity, disrupted circadian patterns, and impaired learning and memory. It results from loss of the fragile X mental retardation 1 protein product (FMRP). A recent study in mice showed that the tetracycline derivative minocycline alleviates FXS symptoms by inhibiting matrix metalloproteinases (MMPs). Siller and Broadie now follow this up with new findings that minocycline treatment restores multiple synaptic connectivity defects in the well-characterised dfmr1-null Drosophila model of FXS. Overexpressing TIMP (an inhibitor of MMP activity) prevents the synaptic connectivity defects in dfmr1-null flies, as does deleting the single MMP present in Drosophila. These data support minocycline as a promising FXS therapy and suggest that the FMRP and MMP pathways interact. Page 673
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