However, given the established crosstalk between mitochondria abnormalities and oxidative stress, and the evidence presented herein including that the hydroxyl free radical scavenger DMSO corrected both CS and ELM-RPE contraction, but not MCP/AR changes in 5xFAD B6J mice, we speculate that a combination of photoreceptor mitochondria dysfunction / oxidative stress / oxidative damage occurs in 5xFAD mice regardless of the presence of Nnt, a rare mutation in humans that leads to familial glucocorticoid deficiency, adrenal insufficiency and hypothyroidism [35, 130–135]. Here, AR is linked to familial glucocorticoid deficiency.