REVIEW article
Front. Neurol.
Sec. Neurogenetics
Volume 16 - 2025 | doi: 10.3389/fneur.2025.1663136
Riboflavin in Neurological Diseases: Therapeutic Advances, Metabolic Insights, and Emerging Genetic Strategies
Provisionally accepted
- Department of Pediatric Neurology, First Affiliated Hospital of Jilin University, Changchun, China
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Background: Riboflavin (vitamin B2), a precursor of flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), is essential for mitochondrial function, redox balance, and neuronal viability. Impairments in riboflavin transport and metabolism contribute to a growing spectrum of neurological diseases. Objective: This review provides a comprehensive update on the therapeutic applications, metabolic mechanisms, and gene-based strategies involving riboflavin in neurological disorders. Methods: We systematically analyzed clinical and experimental studies published between 2012 and 2025, focusing on riboflavin-responsive conditions and molecular mechanisms relevant to neurological pathology. Results: Riboflavin supplementation-particularly in high doses-has demonstrated substantial efficacy in conditions such as riboflavin transporter deficiency (RTD), multiple acyl-CoA dehydrogenase deficiency (MADD), and migraine. Emerging data suggest potential benefit in Parkinson's disease, Alzheimer's disease, multiple sclerosis, and acute brain injury. Mechanistically, riboflavin supports mitochondrial bioenergetics, antioxidant systems, and epigenetic regulation. Recent advances in gene therapy and pharmacological chaperones targeting riboflavin-dependent pathways offer promising therapeutic directions. Conclusion: Riboflavin is evolving from a conventional micronutrient into a multifaceted therapeutic agent in neurology. Integration of gene-based approaches, targeted delivery systems, and biomarker-guided interventions may establish riboflavin as a key component of precision medicine strategies for neurological disorders.
Keywords: Riboflavin, Vitamin B2, Neurological Diseases, Mitochondrial dysfunction, Gene Therapy, Combination therapy 2. Literature Search Strategy
Received: 10 Jul 2025; Accepted: 18 Aug 2025.
Copyright: © 2025 Tao, Huo, Hao and Liang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Jianmin Liang, Department of Pediatric Neurology, First Affiliated Hospital of Jilin University, Changchun, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.