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This cascade of mitochondrial damage, along with the impaired ability of mitochondria to regulate calcium homeostasis and bioenergetics, leads to further neuronal injury and death [157]

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Cell death was increased upon the combined suppression of LDHB expression and GPX4 deletion in A549 cells and could be rescued by both FER1 and mitoTEMPO treatment (Supplementary Fig

Nat Rev Neurosci 12:638651 Kopeikina KJ, Carlson GA, Pitstick R et al (2011) Tau accumulation causes mitochondrial distribution deficits in neurons in a mouse model of tauopathy and in human Alzheimers disease grain