scholarly journals Data on amyloid precursor protein accumulation, spontaneous physical activity, and motor learning after traumatic brain injury in the triple-transgenic mouse model of Alzheimer׳s disease

Data in Brief ◽  
2016 ◽  
Vol 9 ◽  
pp. 62-67 ◽  
Author(s):  
Yasushi Kishimoto ◽  
Hajime Shishido ◽  
Mayumi Sawanishi ◽  
Yasunori Toyota ◽  
Masaki Ueno ◽  
...  
Keyword(s):  
Physical Activity ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Motor Learning ◽  
Mouse Model ◽  
Amyloid Precursor Protein ◽  
Transgenic Mouse Model ◽  
Protein Accumulation ◽  
Spontaneous Physical Activity ◽  
Triple Transgenic Mouse

scholarly journals The Adverse Pial Arteriolar and Axonal Consequences of Traumatic Brain Injury Complicated by Hypoxia and Their Therapeutic Modulation with Hypothermia in Rat

2009 ◽  
Vol 30 (3) ◽  
pp. 628-637 ◽  
Author(s):  
Guoyi Gao ◽  
Yasutaka Oda ◽  
Enoch P Wei ◽  
John T Povlishock
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Amyloid Precursor Protein ◽  
Vascular Reactivity ◽  
Axonal Damage ◽  
Precursor Protein ◽  
Moderate Hypothermia ◽  
Vascular Protection ◽  
Impact Acceleration ◽  
Cerebral Vascular

This study examined the effect of posttraumatic hypoxia on cerebral vascular responsivity and axonal damage, while also exploring hypothermia's potential to attenuate these responses. Rats were subjected to impact acceleration injury (IAI) and equipped with cranial windows to assess vascular reactivity to topical acetylcholine, with postmortem analyses using antibodies to amyloid precursor protein to assess axonal damage. Animals were subjected to hypoxia alone, IAI and hypoxia, IAI and hypoxia before induction of moderate hypothermia (33°C), IAI and hypoxia induced during hypothermic intervention, and IAI and hypoxia initiated after hypothermia. Hypoxia alone had no impact on vascular reactivity or axonal damage. Acceleration injury and posttraumatic hypoxia resulted in dramatic axonal damage and altered vascular reactivity. When IAI and hypoxia were followed by hypothermic intervention, no axonal or vascular protection ensued. However, when IAI was followed by hypoxia induced during hypothermia, axonal and vascular protection followed. When this same hypoxic insult followed the use of hypothermia, no benefit ensued. These studies show that early hypoxia and delayed hypoxia exert damaging axonal and vascular consequences. Although this damage is attenuated by hypothermia, this follows only when hypoxia occurs during hypothermia, with no benefit found if the hypoxic insult proceeds or follows hypothermia.

scholarly journals Acute treatment with TrkB agonist LM22A-4 confers neuroprotection and preserves myelin integrity in a mouse model of pediatric traumatic brain injury

2021 ◽  
Vol 339 ◽  
pp. 113652
Author(s):  
Jessica L. Fletcher ◽  
Larissa K. Dill ◽  
Rhiannon J. Wood ◽  
Sharon Wang ◽  
Kate Robertson ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mouse Model ◽  
Acute Treatment ◽  
Pediatric Traumatic Brain Injury

scholarly journals Peroxynitrite-Mediated Protein Nitration and Lipid Peroxidation in a Mouse Model of Traumatic Brain Injury

2004 ◽  
Vol 21 (1) ◽  
pp. 9-20 ◽  
Author(s):  
Edward D. Hall ◽  
Megan R. Detloff ◽  
Kjell Johnson ◽  
Nancy C. Kupina
Keyword(s):  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Brain Injury ◽  
Mouse Model ◽  
Protein Nitration
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