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With the use of the ASOs to target the SCN1A NAT, one study was effectively able to rescue the sense SCN1A gene expression, ameliorate neuronal excitability and seizures in a mouse model of DSan effect that almost entirely recapitulates the rescued phenotypes observed via CRISPRa treatment [74, 75]

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GIP decreases food intake and increases energy expenditure therefore resulting in weight reduction, and when combined with GLP-1 results in greater effects on markers of metabolic dysregulation such as body weight, glucose, and lipids

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They are endogenously sourced from PPG neurons that are situated caudally in the solitary tract of the brainstem [47, 48]