Parkinson's Disease (PD) is a neurodegenerative disease characterized by the loss of cathecolaminergic neurons of the substantia nigra pars compacta (SNpc), known for its motor symptoms such as bradykinesia and dyskinesia, although it also has its non motor manifestations, mainly respiratory deficits. Those deficits, as seen by Tuppy et. al., showed that rats induced by Parkinson's Disease model present a reduction in the number of neurons from the Pre-Bötzinger and rostral VRG, added to a reduction of chemossensitive neurons of RTN, being those some of the important regions in neural control of breathing, together with a reduction of resting breathing in response to hipercapnia (Tuppy et. al., 2015). Further, Fernandes-Júnior et. al. obtained the same result, analyzing a rise in astroglial activation, cells responsible for the immune surveillance of the neurological system, known for their role in assisting in central chemoreception (Fernandes-Júnior et. al., 2018) Although it is a idiopathic disease, rat models of PD shows an oxidative imbalance of neuronal tissue, including the medullary region of neural control of breathing, which points at a correlation between oxidative stress and respiratory deficits. Starting with the oxidative stress, pro-apoptotic signaling are activated, as our group showed previously. Therefore, having NADPH oxidase (NOX) at hand, an enzyme responsible of producing Reactive Oxygen Species (ROS), we will inhibit it with apocynin, an unspecific inhibitor of NOX, and further analyze of the reversion of the oxidative stress and so, its consequences over the activation of the pro-apoptotic signalling which leads to neurodegeneration. It is going to be evaluated the pro-apoptotic signaling dependent of BAX/Bcl-2 (intrinsic pathway), alongside the Wnt/²-cathenin, a very important pathway responsible for propagation of pro-survival signaling.
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