Astrogliosis is another hallmark of AD pathogenesis.[35] We then determined the level of astrogliosis through glial fibrillary acidic protein (GFAP) immunostaining, finding that the expression of GFAP in the cortex of APP/PS1 mice was 23.33 ± 3.54%, decreased by 68.37% (7.38 ± 0.30%) following RAP‐RL treatment (Figure S8, Supporting Information). This evidence concerns the gene GFAP and Alzheimer disease.