Peripheral mononuclear cell mitochondrial function associates with T-cell cytokines in Parkinson's disease

Background: Parkinson's disease (PD) is the most common neurodegenerative movement disorder and one of the world's fastest-growing neurological diseases. Although the exact causes of PD are unknown, mitochondrial dysfunction and inflammation may have significant roles in disease progression. As well as being prevalent in the brain, there is also evidence that peripheral mitochondrial dysfunction and inflammation occur in PD. However, if/how peripheral mitochondrial dysfunction and inflammation are linked is still unclear. Objectives: This study aimed to determine the extent that mitochondrial dysfunction in peripheral immune cells is associated with inflammation in PD. Methods: The study comprised of 35 controls and 35 PD patients that were age and sex matched. Flow cytometry was used to assess mitochondrial content and superoxide production in mononuclear cells, in the presence and absence of the mitochondrial stressor antimycin A. Serum inflammatory cytokines were measured by ELISA. Results: Superoxide levels were significantly increased in PD patient mononuclear cells at baseline, and PD mononuclear cells had an impaired response to antimycin A. Immune cell superoxide levels correlated with serum cytokines associated with T-cell responses, namely interleukin (IL) IL-12, interferon-γ, and IL-17A. Conclusions: Results show that mitochondrial dysfunction is prevalent in PD immune cells and may contribute to an inflammatory phenotype.