Therefore, the aims of the present study are to test whether the treatment of HLJDT-M substitutes the Aβ increasing effects of HLJDT in 3XTg-AD transgenic mouse model, and on the regulatory processing of APP, thereby demonstrating a significantly more potent treatment for neurodegenerative diseases that does not associate with any Aβ increasing effect. The gene discussed is APP; the disease is Alzheimer disease.