The role of the inflammatory-dependent pathway GSK3b and JAK/STAT in the respiratory nuclei in the Parkinson Disease model of mice after treatment with minocycline.

Abstract

Parkinson's disease (PD) is a degenerative disease characterized by the loss of dopaminergic neurons in the Substantia Nigra. Its motor symptoms are widely known as bradykinesia and dyskinesia, but it also has non classic motor symptoms such as respiratory dysfunction. In rats injected with 6-OHDA in the striatum, a drug that enables the development of a mimetic model of idiopathic PD, there is a loss of neurons in respiratory nuclei such as rotral ventral respiratory group and pre-Bötzinger and significant loss of chemosensitive neurons of the retrotrapezoid nucleus in mice. Studies show that oxidative stress is a major mechanism that explains the decrease in number of these neurons. The presence of reactive oxygen species (ROS) leads to activation of central nervous system immune cells, such as microglia and astrocytes that respond by releasing pro-inflammatory agents that are often toxic to neurons. The aim of this project is to evaluate the GSK3b and JAK/STAT signaling pathways of the inflammatory response in respiratory nuclei using Western Blot technique and microglia reactivity to TNFa using flow cytometry in DP 6-OHDA mice model, and if treatment with minocyclin is able, by inhibiting inflammation in those regions, of preventing respiratory nuclei degeneration and respiratory deficits.