Parkinson’s disease (PD) is the second most common, age-related neurodegenerative disorder in humans. PD is characterized by deterioration of dopaminergic neurons and deposition of Lewy bodies, resulting clinically in tremors, rigidity, slowness with movement and postural instability. Although the exact reasons behind the pathogenesis of PD remains elusive, current research indicates that PD results from complex interactions between genetic, immunological, and environmental factors. Moreover, mitochondrial impairment and oxidative stress are thought to contribute to early stages of PD.
DJ-1 is a protein encoded by the gene PARK7, and appears to protect neurons against oxidative stress and cell death. Defects in the DJ-1 gene or protein are linked to early onset or familial PD. Investigators at Rush University in Chicago have published a study demonstrating that RNS60 is capable of increasing expression of DJ-1 in both an immortalized neuronal cell line and in primary mouse dopaminergic neurons, via activation of the CREB-CBP signaling pathway. These new data support the hypothesis that RNS60 may be of therapeutic benefit for PD and other neurodegenerative diseases where mitochondrial deficits and oxidative stress are involved.