Phosphocreatine (also known as creatine phosphate) has been investigated for its potential neuroprotective effects in Parkinson's Disease (PD) based on its role in cellular energy buffering and mitochondrial function. The rationale comes from the observation that mitochondrial dysfunction and impaired energy metabolism are implicated in PD pathogenesis. Preclinical studies in animal models have shown that creatine supplementation can provide neuroprotection and may slow dopaminergic neuron degeneration. These findings prompted several clinical trials in humans.

However, the clinical evidence supporting the benefit of phosphocreatine or creatine supplementation in PD remains weak. The largest randomized, placebo-controlled trial—the NINDS NET-PD LS-1 study—enrolled over 1,700 patients with early Parkinson’s Disease and tested creatine monohydrate supplementation. The study was halted early due to futility; no significant benefit was observed in slowing disease progression compared to placebo. Other smaller clinical studies have also failed to demonstrate meaningful clinical improvement in PD symptoms with creatine supplementation.

In summary, while there is a mechanistic rationale and supportive preclinical data, current clinical evidence does not support the use of phosphocreatine or creatine to treat or support Parkinson's Disease. Its use is not justified outside of research settings.