scholarly journals Surgical Stress Induces Brain-Derived Neurotrophic Factor Reduction and Postoperative Cognitive Dysfunction Via Glucocorticoid Receptor Phosphorylation in Aged Mice

2015 ◽  
Vol 21 (5) ◽  
pp. 398-409 ◽  
Author(s):  
Xiao-Sheng Tian ◽  
Ya-Wei Tong ◽  
Zheng-Qian Li ◽  
Lun-Xu Li ◽  
Tao Zhang ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Cognitive Dysfunction ◽  
Neurotrophic Factor ◽  
Surgical Stress ◽  
Postoperative Cognitive Dysfunction ◽  
Brain Derived Neurotrophic Factor ◽  
Receptor Phosphorylation ◽  
Aged Mice

Forced running exercise mitigates radiation-induced cognitive deficits via regulated DNA hydroxymethylation

Epigenomics ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 385-396 ◽  
Author(s):  
Junjun Zhang ◽  
Junyan Li ◽  
Yiwen Zhu ◽  
Zhigang Miao ◽  
Ye Tian
Keyword(s):  
Cognitive Dysfunction ◽  
Neurotrophic Factor ◽  
Epigenetic Modification ◽  
Brain Derived Neurotrophic Factor ◽  
Hippocampal Neurogenesis ◽  
Mice Model ◽  
Whole Brain Irradiation ◽  
Running Exercise ◽  
Radiation Induced ◽  
Forced Running

Aim: Roles of forced running exercise (FE) in remediation of neurogenesis inhibition and radiation-induced cognitive dysfunction were investigated in a whole-brain irradiation mice model via the regulation of DNA 5-hydroxymethylation modification (5 hmC) and its catalytic enzymes ten–eleven translocation (Tet) proteins. Materials & methods: Hippocampal neurogenesis and cognitive function, DNA 5 hmC level and Tet expression were determined in mice. Results: The expression of DNA 5 hmC and Tet2, brain-derived neurotrophic factor significantly decreased in hippocampus postradiation. FE mitigated radiation-induced neurogenesis deficits and cognitive dysfunction. Furthermore, FE increased 5 hmC and brain-derived neurotrophic factor expression. SC1, a Tet inhibitor, reversed partly such changes. Conclusion: Tet-mediated 5 hmC modification represents a kind of diagnostic biomarkers of radiation-induced cognitive dysfunction. Targeting Tet-related epigenetic modification may be a novel therapeutic strategy for radiation-induced brain injury.

scholarly journals High-Pressure Pneumoperitoneum Aggravates Surgery-Induced Neuroinflammation and Cognitive Dysfunction in Aged Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Bo Lu ◽  
Hui Yuan ◽  
Xiaojie Zhai ◽  
Xiaoyu Li ◽  
Jinling Qin ◽  
...  
Keyword(s):  
High Pressure ◽  
Cognitive Dysfunction ◽  
Microglial Activation ◽  
Postoperative Cognitive Dysfunction ◽  
Abdominal Pressure ◽  
Common Complication ◽  
Operative Field ◽  
Aged Patients ◽  
Aged Mice ◽  
Postoperative Cognitive Impairment

Postoperative cognitive dysfunction (POCD) is a common complication after surgery, especially in aged patients. Neuroinflammation has been closely associated with the development of POCD. While the contribution of pneumoperitoneum to the systemic inflammation has been well documented, the effect of pneumoperitoneal pressure on neuroinflammation and postoperative cognitive function remains unclear. In this study, we showed that high-pressure pneumoperitoneum promoted the postoperative neuroinflammation and microglial activation in the hippocampus and aggravated the postoperative cognitive impairment in aged mice. These results support the requirement to implement interventions with lower intra-abdominal pressure, which allows for adequate exposure of the operative field rather than a routine pressure.

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