scholarly journals Mild hypothermia reduces endoplasmic reticulum stress‐induced apoptosis and improves neuronal functions after severe traumatic brain injury

2019 ◽  
Vol 9 (4) ◽  
pp. e01248 ◽  
Author(s):  
Chuan‐Fang Wang ◽  
Cheng‐Cheng Zhao ◽  
Yi He ◽  
Zong‐Yang Li ◽  
Wen‐Lan Liu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Endoplasmic Reticulum ◽  
Brain Injury ◽  
Endoplasmic Reticulum Stress ◽  
Severe Traumatic Brain Injury ◽  
Mild Hypothermia ◽  
Induced Apoptosis ◽  
Neuronal Functions

scholarly journals Juvenile Traumatic Brain Injury Results in Cognitive Deficits Associated with Impaired Endoplasmic Reticulum Stress and Early Tauopathy

2018 ◽  
Vol 40 (2) ◽  
pp. 175-188 ◽  
Author(s):  
Michael J. Hylin ◽  
Ryan C. Holden ◽  
Aidan C. Smith ◽  
Aric F. Logsdon ◽  
Rabia Qaiser ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Endoplasmic Reticulum ◽  
Brain Injury ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Short Term ◽  
Behavioral Deficits ◽  
Juvenile Rats ◽  
Tau Oligomers ◽  
Cci Model

The leading cause of death in the juvenile population is trauma, and in particular neurotrauma. The juvenile brain response to neurotrauma is not completely understood. Endoplasmic reticulum (ER) stress has been shown to contribute to injury expansion and behavioral deficits in adult rodents and furthermore has been seen in adult postmortem human brains diagnosed with chronic traumatic encephalopathy. Whether endoplasmic reticulum stress is increased in juveniles with traumatic brain injury (TBI) is poorly delineated. We investigated this important topic using a juvenile rat controlled cortical impact (CCI) model. We proposed that ER stress would be significantly increased in juvenile rats following TBI and that this would correlate with behavioral deficits using a juvenile rat model. A juvenile rat (postnatal day 28) CCI model was used. Binding immunoglobulin protein (BiP) and C/EBP homologous protein (CHOP) were measured at 4 h in the ipsilateral pericontusion cortex. Hypoxia-inducible factor (HIF)-1α was measured at 48 h and tau kinase measured at 1 week and 30 days. At 4 h following injury, BiP and CHOP (markers of ER stress) were significantly elevated in rats exposed to TBI. We also found that HIF-1α was significantly upregulated 48 h following TBI showing delayed hypoxia. The early ER stress activation was additionally asso­ciated with the activation of a known tau kinase, glycogen synthase kinase-3β (GSK-3β), by 1 week. Tau oligomers measured by R23 were significantly increased by 30 days following TBI. The biochemical changes following TBI were associated with increased impulsive-like or anti-anxiety behavior measured with the elevated plus maze, deficits in short-term memory measured with novel object recognition, and deficits in spatial memory measured with the Morris water maze in juvenile rats exposed to TBI. These results show that ER stress was increased early in juvenile rats exposed to TBI, that these rats developed tau oligomers over the course of 30 days, and that they had significant short-term and spatial memory deficits following injury.

Effects of therapeutic mild hypothermia on patients with severe traumatic brain injury after craniotomy

2007 ◽  
Vol 22 (3) ◽  
pp. 229-235 ◽  
Author(s):  
Wusi Qiu ◽  
Ying Zhang ◽  
Hong Sheng ◽  
Jianmin Zhang ◽  
Weiming Wang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Mild Hypothermia ◽  
Therapeutic Mild Hypothermia

scholarly journals Endoplasmic Reticulum Stress Modulation as a Target for Ameliorating Effects of Blast Induced Traumatic Brain Injury

2017 ◽  
Vol 34 (S1) ◽  
pp. S-62-S-70 ◽  
Author(s):  
Brandon P. Lucke-Wold ◽  
Aric F. Logsdon ◽  
Ryan C. Turner ◽  
Jason D. Huber ◽  
Charles L. Rosen
Keyword(s):  
Traumatic Brain Injury ◽  
Endoplasmic Reticulum ◽  
Brain Injury ◽  
Endoplasmic Reticulum Stress
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