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Description

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Mechanistic investigation revealed ChaC1/AUR-driven cytotoxicity was attenuated by disulfide reducing agents (e.g., NAC and TCEP), while maintaining resistance to canonical programmed death pathway inhibitors targeting apoptosis, necroptosis, and ferroptosis

Alzheimers Disease (AD) has been characterized for decades by the presence of histopathological alterations (extracellular amyloid- containing plaques and intracellular tangles of hyperphosphorylated tau-protein) leading to neurodegeneration (synaptic deficits and finally neuronal loss), as well as by severe cognitive deficits

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