In analysis of molecular networks, superoxide dismutase 2 (SOD2), a highly-ranked gene, was found to be upregulated in patients with Parkinson’s disease, allowing researchers to conclude that SOD2 could be a potential blood biomarker for the disease.
In a study published in PLOS One, researchers hoped to further investigate the connection between Parkinson’s disease (PD) and type 2 diabetes, which is associated with more severe forms of PD. Type 2 diabetes (T2DM) contributes to instability, gait difficulty and insulin resistance, which is linked to an increased risk of dementia in PD patients.
Researchers found 84 shared genes between PD and T2DM through genetic database searches, and found that nitric oxide biosynthetic processing, carbohydrate and lipid metabolic processing, insulin secretion, regulation of glucose, and inflammation were the most overrepresented pathways.
After prioritizing the shared genes, SOD2 was found to be the most highly ranked and was found to be upregulated in the blood of PD patients compared to healthy subjects. SOD2 protein levels are often increased in the frontal cortex of PD patients, and increased levels of SOD2 mRNA have been found in the skeletal muscles of T2DM patients.
Additionally, drug therapies meant to treat diabetes have shown promising results in PD patients, including improved motor and cognitive functions. Diabetes therapies are known to interact with SOD2, and therefore observing SOD2 levels in blood can be a useful evaluation of therapeutic effects of diabetes therapies in PD patients.
This study furthers the evidence that Parkinson’s disease and type 2 diabetes share dysregulated molecular networks by identifying 84 shared genes, including SDO2, which is a potential biomarker for Parkinson’s and is known to interact with anti-diabetes drug therapies.