Previous studies have found that the expression level of miR-29a in the cerebrospinal fluid of AD patients is lower than that of the control group, and the decrease of miR-29a can up-regulate the activity of BACE1, induce the production of Aβ protein, lead to excessive deposition of Aβ in the brain tissue, and form the specific pathological markers of AD. Here, BACE1 is linked to Alzheimer disease.