Just as physical exercise strengthens our muscles and cardiovascular system, it turns out that it also has a profound impact on our brain health. A recent study investigated the effects of exercise on cognitive function in rats with chronic cerebral hypoperfusion (CCH), a condition associated with vascular cognitive impairment and dementia. The findings revealed that physical exercise not only improved the rats’ cognitive function but also had a neuroprotective effect through the activation of astrocytes – star-shaped cells in the brain that regulate neuronal activity and maintain brain health. In particular, exercise promoted primary ciliogenesis, which is the formation of tiny hair-like structures on astrocytes that play a crucial role in their function. Furthermore, exercise suppressed the activation of specific signaling pathways, such as ERK and JNK, which are involved in neuroinflammation and neuronal damage. These results suggest that physical exercise could be a promising non-drug treatment for brain disorders associated with CCH and highlights the importance of astrocytes in maintaining brain health. To learn more about this exciting research, check out the full article!

Chronic cerebral hypoperfusion (CCH) is closely related to vascular cognitive impairment and dementia (VCID) and Alzheimer’s disease (AD). The neuroinflammation involving astrocytes is an important pathogenic mechanism. Along with the advancement of the concept and technology of astrocytic biology, the astrocytes have been increasingly regarded as the key contributors to neurological diseases. It is well known that physical exercise can improve cognitive function. As a safe and effective non-drug treatment, physical exercise has attracted continuous interests in neurological research. In this study, we explored the effects of physical exercise on the response of reactive astrocytes, and its role and mechanism in CCH-induced cognitive impairment. A rat CCH model was established by 2 vessel occlusion (2VO) and the wheel running exercise was used as the intervention. The cognitive function of rats was evaluated by morris water maze and novel object recognition test. The phenotypic polarization and the primary cilia expression of astrocytes were detected by immunofluorescence staining. The activation of MAPKs cascades, including ERK, JNK, and P38 signaling pathways, were detected by western blot. The results showed that physical exercise improved cognitive function of rats 2 months after 2VO, reduced the number of C3/GFAP-positive neurotoxic astrocytes, promoted the expression of S100A10/GFAP-positive neuroprotective astrocytes, and enhanced primary ciliogenesis. Additionally, physical exercise also alleviated the phosphorylation of ERK and JNK proteins induced by CCH. These results indicate that physical exercise can improve the cognitive function of rats with CCH possible by promoting primary ciliogenesis and neuroprotective function of astrocytes. The MAPKs signaling cascade, especially ERK and JNK signaling pathways may be involved in this process.

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