The humble vitamin biotin (vitamin B7) has emerged as a potential neuroprotective agent against manganese-induced neurotoxicity linked to Parkinson’s disease (PD). A recent study published in Science Signaling used fruit fly models and human dopaminergic neurons to show that biotin supplementation can reverse neurologic damage caused by excessive manganese exposure. Manganese, though essential at low levels, can become neurotoxic in high concentrations, causing a Parkinson-like syndrome termed manganism. The study’s findings raise intriguing possibilities for developing biotin-based interventions to mitigate manganese toxicity and potentially address aspects of PD.
Researchers have long known that chronic manganese exposure (common in occupations such as welding or mining) leads to neuronal damage resembling PD, including motor deficits and alpha-synuclein aggregation. Manganese also disrupts mitochondria and lysosomes, creating cellular energy deficits and impaired protein clearance. In fruit fly models, manganese exposure caused classic Parkinson-like symptoms—motor impairment, dopaminergic neuron loss, and shortened lifespan—while in human neurons derived from induced pluripotent stem cells (iPSCs), manganese specifically damaged dopaminergic cells.
Enter Biotin. Biotin is best known as a coenzyme that supports metabolic pathways including the Krebs cycle, fatty acid metabolism, and carboxylation reactions critical for energy production. The Science Signaling study describes the observation that manganese exposure disrupted biotin metabolism in flies. That finding suggests biotin’s protective role is more than incidental. What’s more, Supplementing manganese-exposed flies with biotin significantly bolstered their motor function and curbed neurodegeneration. In human dopaminergic neurons, biotin also preserved cell viability and mitochondrial function. That is, it buffers them against manganese’s toxic impact. Conversely, biotin depletion by knocking down the biotinidase gene worsened manganese toxicity.
Mechanisms of neuroprotection
Biotin’s neuroprotective effects likely involve maintaining robust energy production in cells with high metabolic demands—such as dopamine neurons—and reducing oxidative stress. Biotin-dependent enzymes help generate ATP and support myelin integrity. The study also noted that boosting biotin enhanced dopamine synthesis. Because PD pathology includes energy failure, protein misfolding and dopamine neuron loss, biotin’s metabolic support may help neurons resist these stresses. In fruit flies as well as in human neurons, adequate biotin levels appeared essential for sustaining mitochondrial function when challenged by manganese.
Clinical and translational outlook
Though the new data are compelling, clinical evidence for biotin in treating PD or manganism is still scant. No large-scale trials have tested biotin specifically for Parkinson’s or manganese-induced neurotoxicity. Yet high-dose biotin has been studied in progressive multiple sclerosis (MS) with mixed results. Early MS trials suggested possible benefits for disability improvement, but a follow-up Phase 3 trial showed no significant advantage over placebo. These divergent outcomes illustrate the difficulty of translating high-dose vitamin therapies into consistent clinical benefit. Still, biotin generally remains well-tolerated. It can, however, interfere with certain blood tests at high doses.
In PD, interest in biotin also benefits from research showing that people with the disease often have reduced populations of gut bacteria that synthesize B vitamins, including biotin. Restoring biotin levels—through supplements or potentially biotin-producing probiotics—might be beneficial. While such connections are still under investigation, they dovetail with the manganese findings and point to broader metabolic or microbiome strategies for PD management.
As a widely available dietary supplement, biotin is not currently approved as a prescription medication for neurodegenerative diseases. Any attempt to develop it as a drug for PD or manganism would involve conducting rigorous clinical trials to meet regulatory standards for efficacy — obviously without patent protection. Still, the fact that biotin is inexpensive and generally safe might make it more feasible to test in larger human studies.
Filed Under: Brain Breakthroughs, Neurological Disease
