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. 2019 Jun 18;10:635. doi: 10.3389/fneur.2019.00635

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Copyright © 2019 Martin, Wong and Hanaford.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mouse model of mild closed skull cortical contusion injury (CCI) and clinical outcomes. (A) Head of a postnatal day 30 mouse that received a right side CCI (arrow) on postnatal day 7. Surrounding skull muscles and some underlying brain structures, olfactory bulbs (OB) and frontal cortex (frontal), are identified for orientation. Inset shows mild injury to frontal cortex (asterisk) in a cresyl violet-stained section. Scale bar = 238 μm. (B) Acute 48 h mortality of non-transgenic (non-tg) and tg neonatal mouse lines expressing human mutant genes causing human neurodegeneration such as Parkinson's disease (A53T-αSyn), amyotrophic lateral sclerosis (G93A-SOD1), and Alzheimer's disease (APP-PS1). Values shown are mean ± standard deviation (n = 40 mice/group). Asterisks denote significant difference (p < 0.001) compared to non-tg. (C) Motor performance (on running wheel) of 30-day-old mice subjected to sham procedure or CCI at postnatal day 7. Tg A53T-αSyn and G93A-SOD1 mice with CCI had significant deficits in running activity. Values are means ± standard deviation (n = 10/group). Asterisks denote (p < 0.01) compared to sham.