Abstract
Alzheimer’s disease (AD) is characterized by progressive decline of memory and cognitive functions. Deep magnetic stimulation (DMS), a noninvasive and nonpharmacological brain stimulation, has been reported to alleviate stress-related cognitive impairment in neuropsychiatric disorders. Our previous study also discovered the preventive effect of DMS on cognitive decline in an AD mouse model. However, the underlying mechanism must be explored further. In this study, we investigated the effect of DMS on spatial learning and memory functions, neurogenesis in the dentate gyrus (DG), as well as expression and activity of the cholinergic system in a transgenic mouse model of AD (5XFAD). Administration of DMS effectively improved performance in spatial learning and memory of 5XFAD mice. Furthermore, neurogenesis in the hippocampal DG of DMS-treated 5XFAD mice was clearly enhanced. In addition, DMS significantly raised the level of acetylcholine and prevented the increase in acetylcholinesterase activity as well as the decrease in acetyltransferase activity in the hippocampus of 5XFAD mice. These findings indicate that DMS may be a promising noninvasive tool for treatment and prevention of AD cognitive impairment by promoting neurogenesis and enhancing cholinergic system function.
Results:
DMS Rescues Spatial Cognitive Impairment in 5XFAD Mice
DMS Enhances Adult Hippocampal Neurogenesis in 5XFAD Mice
DMS Restores Decreased Ach Levels and ChAT Activity and Increases AchE Activity in the Hippocampus of 5XFAD Mice
Conclusions: Our results suggest that DMS may effectively improve learning and memory performance in 5XFAD mice by restoring cholinergic activity and promoting hippocampal neurogenesis. Furthermore, our findings indicate that DMS could be a new noninvasive therapeutic strategy for AD and other aging-associated cognitive impairments. In the further study, we will expore the probable molecular mechanism of DMS in regulating the neurogenesis.
Keywords: Alzheimer’s disease, hippocampus, cognition, neurogenesis, cholinergic activity
DOI
10.3389/fncir.2017.00048