作者: François V Bolduc , Kimberly Bell , Hilary Cox , Kendal S Broadie , Tim Tully
DOI: 10.1038/NN.2175
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摘要: We used Drosophila olfactory memory as a model to study the molecular basis of cognitive defects in Fragile X syndrome vivo. observed that fragile protein was acutely required and interacted with argonaute1 staufen formation long-term memory. Occlusion mutants could be rescued by synthesis inhibitors, suggesting excess baseline negatively affect cognition.