Sodium butyrate, a short-chain fatty acid and histone deacetylase (HDAC) inhibitor, has been studied in preclinical models for its potential neuroprotective effects in Parkinson's Disease (PD). Animal studies suggest that sodium butyrate may reduce neuroinflammation, decrease oxidative stress, and protect dopaminergic neurons by modulating gene expression through epigenetic mechanisms. Several rodent studies have demonstrated that sodium butyrate administration can improve motor function and reduce dopaminergic neuron loss in toxin-induced models of PD (e.g., MPTP or 6-OHDA models).

The rationale for its use is grounded in the observation that butyrate can cross the blood-brain barrier, influence neurotrophic factors (such as BDNF), and alter the gut microbiome, which may play a role in PD pathophysiology. However, as of June 2024, there is no robust evidence from human clinical trials demonstrating efficacy or safety of sodium butyrate for treating or supporting Parkinson's Disease patients. The current evidence is limited to animal and in vitro studies. Thus, while the use of sodium butyrate is supported by scientific rationale and preliminary preclinical findings, it lacks strong clinical validation.

In summary, sodium butyrate is being investigated for PD based on mechanistic and animal data, but its use in humans remains experimental and unproven.