Mitochondrial Ferritin Deletion Exacerbates β-Amyloid-Induced Neurotoxicity in Mice

Figure 6

A schematic representation of the mechanism leading to neuronal cell apoptosis induced by A in mice with a disrupted Ftmt gene. A changes the levels (LIP) and distribution of intracellular iron, thus increasing oxidative stress. Without Ftmt to sequester excess mitochondrial iron, lipid peroxidation and the level of LIP are significantly increased. These changes may signal the cell to begin the process of programmed death through the P38 MAPK pathway, resulting in neuronal cell death, which is enhanced in Ftmt knockout mice, leading to worsened memory impairments.