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This suggests that the pathological processes and tissue damage established over years of CFTR dysfunction may not be entirely reversible by the current levels of CFTR correction achieved, or that the restoration of CFTR function is insufficient to fully extinguish these self-perpetuating cycles of inflammation and oxidative damage

Understanding the dose-response relationship is essential for designing appropriate research protocols [9]

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In primary neurons, endogenously synthesized -glutamylcysteine fully prevents apoptotic death in several neurotoxic paradigms and, in an in vivo mouse model of neurodegeneration, -glutamylcysteine protects against neuronal loss and motor impairment