For example, activated JNK and P38 are highly expressed in the brains of AD patients (Area-Gomez et al., 2018), JNK also co-localizes with Aβ (Song et al., 2018), and the activation of JNK in APP/PS1 double transgenic mice resulted in a significant increase in senile plaques and neurogenic fibrillary tangles, as well as neuronal apoptosis (Fang et al., 2018). This evidence concerns the gene APP and Alzheimer disease.