Exercise combined with cognitive rehabilitation training affects miR-103a-3p/BDNF expression to improve Alzheimer’s disease

Abstract Objectives Exercise and cognitive rehabilitation exercises (EC) have been shown to slow the progression of Alzheimer’s disease (AD). To evaluate the regulation of EC for the miR-103a-3p/BDNF expression to delay the progression of AD. Methods AD patients were assigned to control (n=30) and EC groups (n=30) using a random number table method. Cognition was assessed using the Mini-Mental State Examination (MMSE), ‌Activity of Daily Living (ADL), and the Alzheimer’s Disease Assessment Scale–Cognition (ADAS-Cog) before and after treatment.in AD patients. The expression of miR-103a-3p in AD patients was detected by the RT-qPCR method. The expression of amyloid β-protein (Aβ), phosphorylated Tau proteins (p-Tau), BDNF, Tumor Necrosis Factor-α (TNF-α), and Interleukin-1 beta (IL-1β) in the serum of AD patients was measured by ELISA. Results After six months of EC treatment for them, MMSE and ALD scores were elevated, and ADAS-cog scores were reduced in AD patients. In addition, serum Aβ 1-42 was elevated and p-Tau was decreased in AD patients after EC treatment. RT-qPCR results indicated that the expression of miR-103a-3p was reduced in AD patients after EC treatment. The results of ELISA indicated that the expression of BDNF was increased while TNF-α and IL-1β were decreased in AD patients after EC treatment. Dual-luciferase reporter assay confirmed miR-103a-3p targeting of BDNF. Conclusions EC may affect miR-103a-3p/BDNF expression to inhibit the expression of pro-inflammatory factors (TNF-α and IL-1β), thus alleviating AD.