University thesis:
Dissertation, Georg-August-Universität Göttingen, 2019
Footnote:
Description:
This work should address the question of whether mitochondrially-generated ROS are the possible cause of neuronal dysfunction in RTT. Data collected in previous studies suggest that oxidative stress is important for the disease progression. Since mitochondria, as "cell power plants", contribute significantly to the production of ROS, possible increased ROS levels in MeCP2-deficient neurons have also been sought under physiological stimulation. The results indicate that the mitochondria, due to their overall comparatively weak redox responses, are only partially responsible for ROS-induced c...