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Initial characterization of the glutamate-cysteine ligase modifier subunit Gclm(-/-) knockout mouse

It's noteworthy that these Parkinson-like events following ranibizumab administration are distinguished by the absence of cortical and subcortical atrophy, suggesting a unique pathophysiological mechanism distinct from typical PD presentations (Sultana and Scondotto 2020)

These antiapoptotic mechanisms constitute vulnerabilities and, consequently, targeting them with either BCL2 family inhibitors 24,25,34 or via suppression of cFLIP 26 kills senescent cells