The Potential Neuroprotective Role of Biotin in Neurorehabilitation: A Review

Purpose of Review: Biotin is a water-soluble vitamin that mammals cannot synthesize and must obtain from the diet. Beyond its established role as a cofactor for biotin-dependent carboxylases, biotin has attracted neurological interest because intermediary metabolism, lipid handling, and myelin maintenance are biologically linked. This narrative review examines biotin across three distinct exposure contexts—nutritional adequacy, functional insufficiency, and pharmacological supplementation—and evaluates its putative relevance to neuroprotection and neurorecovery-oriented processes. Recent Findings: Dietary biotin intake is generally sufficient in mixed diets, and overt deficiency is uncommon; however, low diet quality, reduced bioavailability, and methodological limitations in status assessment may complicate interpretation of biotin sufficiency in clinical nutrition. No validated gold-standard biomarker is currently available. Experimental studies suggest that biotin may modulate pathways related to cellular bioenergetics, lipid metabolism, and myelin-associated processes, but these findings are predominantly preclinical and should not be interpreted as direct evidence of clinical efficacy. In progressive multiple sclerosis, high-dose biotin has been evaluated in human studies, including randomized trials, yet clinical results remain inconsistent and laboratory assay interference remains a relevant practical limitation. Summary: Current evidence does not support conflating adequate dietary biotin intake with pharmacological high-dose exposure. Although biotin remains mechanistically plausible in neuroenergetics and myelin-related disorders, its therapeutic relevance to neurorecovery remains uncertain. Better-designed studies are needed to refine exposure assessment, define dose–response relationships, and determine whether mechanistic signals translate into meaningful clinical benefit.