Toward a therapeutic intervention of lissencephaly, we applied a novel calpain inhibitor, SNJ1945. Peri-natal or post-natal treatment with SNJ1945 rescued defective neuronal migration in Lis1+/− mice, impaired behavioral performance and improvement of 18F-FDG uptake. Furthermore, SNJ1945 improved the neural circuit formation and retrograde transport of NFG in Lis1+/− mice. Thus, SNJ1945 is a potential drug for the treatment of human lissencephaly patients.
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