The Potential Neuroprotective Role of Biotin in Neurorehabilitation: A 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.

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. 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.