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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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Early-life brain trauma accelerates the development of later-life PD and proteinopathy in mutant A53T-αSyn Tg mice. (A) PD-like disease onset occurs significantly (^*p < 0.01) earlier in mutant A53T-αSyn Tg mice with postnatal day 7 CCI compared to sham-procedure mutant A53T-αSyn Tg mice. Values are mean ± SD (n = 10 mice/group). (B) Kaplan-Meier plot showing that PD-like disease onset, neurological decline, and death occur earlier in mutant A53T-αSyn Tg mice with postnatal day 7 CCI compared to sham-procedure mutant A53T-αSyn Tg mice. (C) Western blotting shows advanced hαSyn oligomerization in forebrain at 3 months of age in mutant A53T-αSyn Tg mice with postnatal day 7 CCI compared to naïve and sham-procedure mutant A53T-αSyn Tg mice. Synaptophysin (Synapto) immunoblot shows protein loading. (D) Western blotting shows advanced hαSyn nitration in forebrain at 3 months of age in mutant A53T-αSyn Tg mice with postnatal day 7 CCI compared to age-matched sham-procedure mutant A53T-αSyn Tg mice and mutant A53T-αSyn Tg mice with CCI at 24 h. Ponceau S-stained membrane shows protein loading.