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Since increased -tubulin acetylation has been reported to interact with S and stabilises microtubules (Jensen et al., 2000), it could be possible that increased acetylated -tubulin stimulates S aggregations through its affinity to microtubules (Outeiro et al., 2007) and promotes cell death

Although current dosage studies remain insufficient, future research conducted under GRAS and FDA/EFSA frameworksfocusing on doseresponse relationships and long-term safety evaluationswill help ensure both therapeutic efficacy and patient adherence

Thereby suggesting a promising avenue for their utilization in the treatment of inflammatory disorders [72]

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