Cognitive improvement of mice induced by exercise prior to traumatic brain injury is associated with cytochrome c oxidase

2014 ◽  
Vol 570 ◽  
pp. 86-91 ◽  
Author(s):  
Ying li Gu ◽  
Li wei Zhang ◽  
Ning Ma ◽  
Lin lin Ye ◽  
De xin Wang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Cognitive Improvement

Traumatic Brain Injury-Induced Changes in Gene Expression and Functional Activity of Mitochondrial Cytochrome C Oxidase

2001 ◽  
Vol 18 (10) ◽  
pp. 993-1009 ◽  
Author(s):  
L.K. Harris ◽  
R.T. Black ◽  
K.M. Golden ◽  
T.M. Reeves ◽  
J.T. Povlishock ◽  
...  
Keyword(s):  
Gene Expression ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Functional Activity ◽  
Mitochondrial Cytochrome ◽  
Induced Changes ◽  
Mitochondrial Cytochrome C

scholarly journals Analysis of the Changes in the Oxidation of Brain Tissue Cytochrome-c-Oxidase in Traumatic Brain Injury Patients during Hypercapnoea

2011 ◽  
pp. 9-14 ◽  
Author(s):  
Ilias Tachtsidis ◽  
Martin M. Tisdall ◽  
Caroline Pritchard ◽  
Terence S. Leung ◽  
Arnab Ghosh ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Brain Tissue

scholarly journals CD95/Fas mediates cognitive improvement after traumatic brain injury

Cell Research ◽  
2007 ◽  
Vol 17 (8) ◽  
pp. 732-734 ◽  
Author(s):  
Christoph P Beier ◽  
Martina Kölbl ◽  
Dagmar Beier ◽  
Chris Woertgen ◽  
Ulrich Bogdahn ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Improvement

scholarly journals EVALUATION OF THE MITOCHONDRIA RESPIROMETRIC FUNCTION IN THE CONDITIONS OF PATHOLOGIES OF VARIOUS GENESES

2019 ◽  
Vol 7 (1) ◽  
pp. 20-31 ◽  
Author(s):  
A. V. Voronkov ◽  
D. I. Pozdnyakov ◽  
S. A. Nigaryan ◽  
E. I. Khouri ◽  
K. A. Miroshnichenko ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Ischemia ◽  
Cytochrome C ◽  
Mitochondrial Respiration ◽  
Respiratory Function ◽  
Focal Cerebral Ischemia ◽  
Muscle Dysfunction ◽  
Nadph Oxidase 4

The aim of the paper is to assess the change in the mitochondrial respirometric function under conditions of various pathologies.Materials and methods. The study was performed on male Wistar rats. Experimental focal cerebral ischemia, traumatic brain injury, coronary occlusive myocardial infarction and muscle dysfunction were used as pathological models. Focal ischemia was reproduced by the method of irreversible thermocoagulation of the middle cerebral artery. Traumatic brain injury was modeled by the method of free fall of the load. Experimental myocardial infarction was reproduced by ligating the descending branch of the left coronary artery. Muscle dysfunction was modeled by the method of «forced swimming with a 20% burden». The respiratory function of mitochondria was assessed by the method of respirometry by the change in oxygen consumption when introducing mitochondrial respiration into the medium: Oligomycin, Rotenone and FCCP. Additionally, we evaluated the intensity of the glycolysis process and the activity of respiratory complexes I, II, IV and V. In order to comprehensively assess the respiratory function, an ELISA study was conducted to determine the concentration of ATP, mitochondrial ATP synthetase, cytochrome C oxidase and NADP-Oxidase 4.Results. In the course of the study it was established that under conditions of experimental cerebral ischemia, traumatic brain injury, myocardial infarction and muscle dysfunction, the ATP-generating ability of mitochondria the maximum breathing and respiratory capacity deteriorated, herby the decrease in overall respiratory function was accompanied by an increase in glycolysis, which was uncompensated, as well as dysfunction of mitochondrial complexes I, II, IV and V, confirmed by an increase in NADPH oxidase 4 activity and a decrease in cytochrome C oxidases and ATP synthetase. As a result, the observed changes in mitochondrial respiration function contributed to a decrease in ATP concentration under conditions of cerebral ischemia - by 3.2 times (p <0.05), traumatic brain injury – by 2.6 times (p <0.05), myocardial infarction – by 1.8 times (p <0.05) and muscle dysfunction – by 4 times (p <0.05).Conclusion. Basing on the data obtained, we can assume that in conditions of cerebral ischemia, traumatic brain injury, myocardial infarction and muscle dysfunction, there is deterioration of the mitochondrial respirometric function with inhibition of ATP synthesis and increased glycolysis.

Examining Cogmed's Impact on the Cognitive Improvement of Individuals with Traumatic Brain Injury

2021 ◽  
Vol 102 (10) ◽  
pp. e120
Author(s):  
Brooks Peterson ◽  
Jessica Frias ◽  
Isaac Tourgeman
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Improvement

Cytochrome c release and caspase activation after traumatic brain injury

2002 ◽  
Vol 949 (1-2) ◽  
pp. 88-96 ◽  
Author(s):  
Patrick G Sullivan ◽  
Jeffrey N Keller ◽  
Wendy L Bussen ◽  
Stephen W Scheff
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cytochrome C ◽  
Caspase Activation ◽  
Cytochrome C Release

scholarly journals Inhibition of the integrated stress response reverses cognitive deficits after traumatic brain injury

2017 ◽  
Vol 114 (31) ◽  
pp. E6420-E6426 ◽  
Author(s):  
Austin Chou ◽  
Karen Krukowski ◽  
Timothy Jopson ◽  
Ping Jun Zhu ◽  
Mauro Costa-Mattioli ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Stress Response ◽  
Cognitive Deficits ◽  
Memory Deficits ◽  
Translation Initiation Factor ◽  
Integrated Stress Response ◽  
Physiological Level ◽  
Cognitive Improvement

Traumatic brain injury (TBI) is a leading cause of long-term neurological disability, yet the mechanisms underlying the chronic cognitive deficits associated with TBI remain unknown. Consequently, there are no effective treatments for patients suffering from the long-lasting symptoms of TBI. Here, we show that TBI persistently activates the integrated stress response (ISR), a universal intracellular signaling pathway that responds to a variety of cellular conditions and regulates protein translation via phosphorylation of the translation initiation factor eIF2α. Treatment with ISRIB, a potent drug-like small-molecule inhibitor of the ISR, reversed the hippocampal-dependent cognitive deficits induced by TBI in two different injury mouse models—focal contusion and diffuse concussive injury. Surprisingly, ISRIB corrected TBI-induced memory deficits when administered weeks after the initial injury and maintained cognitive improvement after treatment was terminated. At the physiological level, TBI suppressed long-term potentiation in the hippocampus, which was fully restored with ISRIB treatment. Our results indicate that ISR inhibition at time points late after injury can reverse memory deficits associated with TBI. As such, pharmacological inhibition of the ISR emerges as a promising avenue to combat head trauma-induced chronic cognitive deficits.

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