Physical exercise reserved amyloid-beta induced brain dysfunctions by regulating hippocampal neurogenesis and inflammatory response via MAPK signaling

• DOI: 10.1016/j.brainres.2018.04.040
• Publication Date: 2018-05-02T19:49:21Z
• Authors: Li-na Sun; Jin-shun Qi; Rong Gao
• Keywords: BETA (programming language); Amyloid beta; Amyloid (mycology)

Alzheimer's disease (AD) is one of the leading causes of dementia that induced by aggregation of amyloid-beta (Aβ) in brain tissue. With high structural and functional plasticity, hippocampus plays fundamental roles in cognitive regulation. Moreover, impaired hippocampal functions present during early onset of AD. Hence, targeting on improving hippocampal plasticity would be recognized as the effective strategy in AD therapy. Physical exercise is widely encouraged healthy life style. However, whether exercise could reserve the neural dysfunctions in AD model and the possible neurobiological mechanism still need for better understanding. In current study, we created the AD model by intra-hippocampal injection of Aβ. Afterward, mice were administrated with treadmill running to mimic the physical exercise. Our results show that physical exercise prevented the Aβ-induced cognitive deficits in object recognition task and the Morris water maze. Morphological studies reveal physical exercise increased the adult neurogenesis and release the immune-response in hippocampal dentate gyrus (DG) region. In addition, physical exercise released the immune-response by decreasing the level of cytokines and population of astrocytes that elevated by injection of Aβ. We also found that physical exercise changed the modification of ERK, p38 and JNK, which recognized as the representative MAPK signaling involving with hippocampal neural functions. In conclusion, exercise serves as a potential strategy to prevent the development of AD by regulating adult neurogenesis and brain immune-activity via controlling MAPK signaling.