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A new study found that combining two treatments—one that fixes the faulty SMN2 gene and another that blocks an enzyme called HDAC6—greatly improved muscle strength and survival in a mouse model of spinal muscular atrophy (SMA). This is important because it offers a potential way to help SMA patients who still face muscle weakness even after receiving newer gene therapies.
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A new serum biomarker emerges for the prodromal phase of Alzheimer’s disease
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A New Neural Blueprint for Predicting the Future
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