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. 2018 Sep 4;11:318. doi: 10.3389/fnmol.2018.00318

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Copyright © 2018 Hofer, Kainz, Zimmermann, Bauer, Pendl, Poglitsch, Madeo and Carmona-Gutierrez.

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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Therapeutic approaches to tackle toxicity and/or aggregation in yeast models of HD. Yeast has long served as a tool to identify pharmacological agents against HD. Here, important processes (aggregation and kynurenine pathway) of HD toxicity in yeast are depicted. Prominent approaches previously used in yeast are the application of the polyphenol epigallocatechin-3-gallate (EGCG), intrabodies or the small molecule C2-8, all in order to reduce intracellular aggregation load. The KMO inhibitor Ro 61-8048 was used to modulate the course of tryptophan degradation via the kynurenine pathway, which is heavily implicated in HD, leading to less cell death. AB (here intrabody), EGCG (epigallocatechin-3-gallate), KMO (kynurenine 3-monooxygenase).