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These data are highly significant to AD because: (1) mitochondrial dysfunction (Selfridge et al., 2013) and calpain-activation are linked to AD (Saito et al., 1993

However, when performing a similar pH titration with the U597C variant minimal changes in the formation of the thiolate-FAD charge transfer are observed (Figure 9A) suggesting both that the 571 histidine residue is the acting general base and the C159 residue is highly shielded from solvent

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Mitochondrial impairment severely compromises the ability of the brain to form memories by disrupting energy supply, calcium balance, and synaptic plasticity (Walters and Usachev, 2023)