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. 2019 Jul 22;55(7):396. doi: 10.3390/medicina55070396

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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AASs vs. sport exercise: The latter determines important anti-apoptotic and pro-proliferative functions on the hippocampus, implicated in anxiolytic control. AAS consumption blocked this effect, likely via brain-derived neurotrophic factor (BDNF), mRNA expression is inversely dependent on AAS use. Moreover, exercise seems to not be capable of repairing hippocampal AAS-induced damage. The result is a significant lowering of the hippocampal levels of BDNF, reducing adaptability to stress and neurotrophism.