Accumulating evidence has demonstrated that Sod1-deficient (Sod1−/−) mice show complete SOD1 protein loss and increased intracellular O2•− as well as various aging-associated organ pathologies, such as hepatic carcinoma [3], fatty liver [4], acceleration of Alzheimer’s disease [5,6], macular degeneration [7,8], dry eye [9,10], hemolytic anemia [11], osteopenia [12,13], skin atrophy [14,15], skeletal muscle atrophy [16], luteal degeneration [17], and alteration of the gastrointestinal microbiota [18]. This evidence concerns the gene SOD1 and early-onset autosomal dominant Alzheimer disease.