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. 2020 Dec 22;14:617327. doi: 10.3389/fnbot.2020.617327

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Copyright © 2020 Deng, Zhong, Zhao, He, Lian, Jiang and Chen.

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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Graphical Abstract — Graphical abstract of the role of Gal3 in HD pathogenesis. The level of Gal3 expressed by microglia is low under normal conditions. In HD patients, mutant Huntingtin (mHTT) continues to accumulate due to Huntingtin (HTT) mutations and NFκB is activated. NFκB triggers Gal3 aggregation, while Gal3 feedback promotes NFκB activation. mHTT causes lysosome damage, but Gal3 prevents the damaged lysosome from being cleared. NLRP3Inflammasome and proinflammatory factors (such as IL1β) increase in number, causing neuronal death and repair of damage.