This 12 month, single-case study was predicated on a mouse model of AD (the CVN-AD model; Colton et al., 2008, 2014; Wilcock et al., 2014; Kan et al., 2015), which reduced the levels of iNOS in mice to mimic human levels, resulting in a mouse model that mirrored the course of human AD, beginning with asymptomatic amyloidosis and followed by hyperphosphorlyated tau, age-dependent hippocampal neuronal loss, and behavioral changes in episodic memory and executive function. This evidence concerns the gene MAPT and amyloidosis.