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. 2020 Jul 30;14:761. doi: 10.3389/fnins.2020.00761

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Copyright © 2020 Ledreux, Pryhoda, Gorgens, Shelburne, Gilmore, Linseman, Fleming, Koza, Campbell, Wolff, Kelly, Margittai, Davidson and Granholm.

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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Schematic representation of exosome biology in a normal cell (A) and after mTBI (B). Normally, endocytosis (A) leads to inclusions of early endosomes (B), which in turn leads to development of multivesicular bodies (MVB, C), which can either be demolished by the lysosomal pathway (D), or expelled from the cell as exosomes (E). Studies suggest that after a TBI the lysosomal/autophagosomal pathway is increased, to the detriment of exosomal secretion. Autophagosomal markers, such as LC3 are elevated.