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Mutation, deletion or inactivation of the gene that encodes ALS in humans and mice decreases circulating levels of IGF-1 and IGFBP-3, causing moderate growth deficiency and abnormalities in bone and carbohydrate metabolism

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Moving forward, research should prioritize the integration of insights across preventative and therapeutic domains, fostering synergistic connections between diverse strategies to address these diseases with enhanced precision and efficacy, ultimately leading to improved diagnostic accuracy, treatment experiences, and sustained benefits for patients

Future large-scale, multicenter trials with standardized protocols are essential to validate these findings and facilitate the integration of natural products into mainstream AD treatment frameworks