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Small-molecule agonists of TrkB (e.g., 7,8-dihydroxyflavone) can penetrate the blood-brain barrier and potentially activate BDNF signaling while supporting mitochondrial function [120], but their specificity and long-term safety in humans remain questionable, and they do not address the fundamental barrier of blood-brain barrier penetration for large-molecule NTFs (e.g., GDNF)

For years, skeptics argued that taking glutathione orally was ineffective because the digestive system is designed to break down proteins

These mechanisms include changes in microbial composition, immune activation, vagus nerve signaling, and the production of specific microbial neuroactive metabolites (197)

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