What is the impact of mitochondrial dysfunction and subsequent oxidative stress in central nervous system pathology?

Sperlagh CopieDuring Glycation World Congress, Dr Beata Sperlagh from the Hungarian Academy of Sciencees will present her recent study about the development of a novel series of potent and selective MAO-B inhibitory (hetero)arylalkenylpropargylamine compounds having also protective properties against the supra-additive effect of mitochondrial dysfunction and oxidative stress. 

Mitochondrial dysfunction, oxidative stress and their interplay are core pathological features of neurodegenerative diseases. In Parkinson's disease (PD), mitochondrial dysfunction and oxidative stress have a supra-additive impact on the pathological, cytoplasmic accumulation of dopamine and its subsequent release. Moreover, dopamine and their metabolites provide an additional source of reactive oxygen species (ROS) during their breakdown by monoamine oxidase or auto-oxidation.

Therefore those drugs which simultaneously target mitochondrial dysfunction, oxidative stress and subsequent pathological dopamine release may have disease-modifying potential in addition to symptomatic improvement by the blockade of self-amplifying circuits leading to ROS generation. 

If you are interested to know more about Dr Sperlagh's study, don't hesitate to register on www.glycation-site.com