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. 2024 Apr 2;13:17. doi: 10.1186/s40035-024-00406-z

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Model of mechanisms underlying the therapeutic potential of time-restricted eating in Huntington’s disease (HD). Scheduled daily eating and fasting, known as time-restricted eating (TRE), in HD and non-HD human and animal studies reveals that the practice increases autophagic activity which is thought to decrease aggregation of the mutant huntingtin protein (mHTT), stimulates production of brain-derived neurotrophic factor (BDNF), improves metabolic functions, promotes oxidative stress resistance, decreases reactive oxygen species (ROS), and improves measures of circadian rhythm function. Created with BioRender.com