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Prevention

As of 2024, no disease-modifying therapies exist that reverse or slow neurodegeneration, processes respectively termed neurorestoration and neuroprotection. However, several factors have been found to be associated with a decreased risk. The identification and mechanistic analysis of these factors may guide the development of new therapies.

Exercise—one of the most common recommendations to prevent or delay Parkinson's—may exert a neuroprotective effect. In animal studies investigating the cellular basis, exercise has been found to increase neurotrophic growth factor expression and to reduce alpha-synuclein expression, neuroinflammation, and mitochondrial dysfunction.

Tobacco use and smoking is strongly associated with a decreased risk, reducing the chance of developing PD by 40–60%. Various tobacco and smoke components have been hypothesized to be neuroprotective, including nicotine, carbon monoxide, and monoamine oxidase B inhibitors. Consumption of coffee, tea, or caffeine is also strongly associated with neuroprotection. In laboratory models, caffeine has been shown to be neuroprotective due to its antagonistic interaction with the adenosine A receptor, which modulates dopaminergic signaling, synaptic plasticity, synapse formation, and inflammation. Perscribed adrenergic antagonists like terazosin may also reduce risk.

Although findings have varied, usage of nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen may be neuroprotective. Calcium channel blockers (CCB) may also have a protective effect, with a 22% risk decrease found in a 2024 meta-analysis of almost 3 million CCB users. Higher blood concentrations of urate —a potent antioxidant —has been proposed to be neuroprotective; animal and cell studies have shown that urate can prevent dopaminergic neurodegeneration. Although longitudinal studies observe a slight decrease in PD risk among those who consume alcohol —possibly due to alcohol's urate-increasing effect—alcohol abuse may increase risk.