Furthermore, studies using cell lines and mouse models harboring genetic mutations linked to familial AD, have demonstrated that a compromised mitochondrial antioxidant defense, unable to handle mitochondrial-derived ROS, promotes the amyloidogenic pathway and the activity of MAPT/TAU-related kinases, thus contributing to establish a vicious cycle of oxidative stress and damage [44,98,99]
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As part of nutritional immunity, the host restricts bacterial access to Mn by either sequestering Mn with calprotectin or by increasing zinc (Zn) levels, which compete with Mn for bacterial uptake, both of which can lead to Mn starvation in bacteria and inhibit bacterial growth (Morey et al., 2015)
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