Thus, features such as oxidative damage associated with mitochondrial dysfunction [52] that cause the overproduction of amyloid precursor protein (APP) processing [53] and pathological accumulations of hyperphosphorylated tau [54], which are implicated in age-dependent cognitive decline [55], made SAMP8 a suitable mouse model to evaluate the effects of the natural product mixture treatment for AD. Here, APP is linked to Alzheimer disease.