Unraveling Riboflavin-Mediated Mitochondrial Modulation as a Therapeutic Pathway in Neurological Disorders: An Integrative Systematic Review.
Level 1 - systematic review of randomized trials
Systematic review encompassing clinical trials alongside preclinical studies
PubMed 41720188 · doi:10.1016/j.tjnut.2026.101427
What was done
A systematic review was conducted across PubMed, Embase, Scopus, and Web of Science databases to evaluate riboflavin's therapeutic role and molecular mechanisms via mitochondrial modulation in neurological disorders. The review synthesized 23 eligible studies, comprising 6 in vitro studies, 10 rodent models, and 7 clinical trials across monogenic mitochondrial disorders, neurodegenerative diseases, demyelinating conditions, hypoxic/cerebrovascular injury, and pain or migraine.
What was found
The abstract reports qualitative observations without specific numerical outcomes or pooled effect estimates. Clinical evidence indicated riboflavin may modulate oxidative stress in stroke and perinatal asphyxia with functional gains. Preclinical studies reported reduced α-synuclein aggregation in Parkinson's disease models, increased tyrosine-hydroxylase-positive neurons in Alzheimer's disease models, enhanced neuronal survival in Brown-Vialetto-Van Laere and Huntington's disease models, and normalized neuronal excitability in ataxia and migraine models. No therapeutic effects were found in demyelinating diseases.
Why it matters
This review outlines the mitochondrial and redox mechanisms of riboflavin across neurological indications, highlighting that despite promising preclinical rationale, clear human clinical dosage regimens currently exist only for stroke and migraine.
Limits
The abstract provides no numerical data, effect sizes, or formal meta-analytic pooling. Most included evidence is preclinical (16 of 23 studies were animal or in vitro models), clinical sample sizes and specific trial methodologies are not detailed in the abstract, and riboflavin demonstrated no therapeutic effect in demyelinating conditions.
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- context Evidence shows that supporting mitochondria with cofactors including vitamin B2, vitamin B3, and magnesium is beneficial in Parkinson's disease.