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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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The Disconnected Brain: How MS Severity Differs by Race
The metabolic cost of comfort: how obesity rewires the brain’s stress response
A new consensus sharpens the view on cerebrovascular crises
Un modelo de visión artificial para clasificar enfermedades musculares desde la histopatología
Rituximab offers a new therapeutic avenue for IgA vasculitis
Rituximab offers a new therapeutic avenue for IgA vasculitis
The X Factor in Disease: Sex Chromosomes Reveal Differential Risks
The brain’s social ladder: how dominance reshapes neural architecture
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