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6 Conclusion DS, a severe neurodevelopmental disorder dominated by SCN1A dysfunction, exhibits profound mechanistic complexity: SCN1A mutations disrupt Nav1.1 expression in GABAergic interneurons through transcriptional dysregulation, pre-mRNA splicing defects, and voltage-gated sodium channel dysfunction, leading to impaired inhibitory synaptic transmission and brainwide excitatory-inhibitory imbalance

Coupled with a decline in physical activityattributable to the sedentary nature of many modern occupations, changes in modes of transportation, and the rise of urban livingthis shift has led to a significant energy imbalance

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At first, by increasing QA levels under inflammatory condition, NAD + levels increase, however after saturation of converting enzyme and increase in oxidative activity induced by QA, there is a drop in NAD + production

Khoshkam et al