A new preclinical study suggests THC may induce mitochondrial biogenesis, an effect that could slow the progression of Parkinson’s disease. In the study, which was published in Oncotarget, researchers from Plymouth University Peninsula Schools of Medicine and Dentistry looked at the neuroprotective properties of THC when administered to human neuroblastoma SH-SY5Y cell models. Their findings suggest THC interacts with proliferator-activated receptor γ (PPARγ), or the glitazone receptor, to elicit a chemical reaction that induces mitochondrial biogenesis, restores mitochondrial content, and therefore offers neuroprotection. The researchers even determined THC offered greater neuroprotection than the commonly known PPARγ agonist pioglitazone, which has been known to offer neuroprotective benefits in both animal and cell culture studies of Parkinson’s disease. THC even induced mitochondiral biogensis to reverse deficits, something pioglitazone has not been found to do. This may be because the neuroprotection offered by both compounds are elicited via different pathways. The two compounds offered the greatest neuroprotective effects and greatly reduced neuronal death when working in tandem with each other.
Researchers concluded, “Our data indicate that rather than reducing oxidative stress by PPARγ-regulated expression… THC induces PPARγ-mediated mitochondrial biogenesis whilst pioglitazone, whose protective effect is most likely only partially driven by PPARγ, does not. Indeed our data suggest that Δ9-THC can add to the neuroprotective effect of pioglitazone… THC is generally well tolerated by [Parkinson’s disease] patients and may therefore represent an alternative worthy of consideration… Furthermore, the ability of Δ9-THC to induce mitochondrial biogenesis is interesting as decreased mitochondrial content has been associated with familial as well as sporadic cases of [Parkinson’s disease].”