Journal article
Dietary fasting and time-restricted eating in Huntington's disease: therapeutic potential and underlying mechanisms
Translational neurodegeneration, Vol.13(1), pp.17-13
04/02/2024
DOI: 10.1186/s40035-024-00406-z
PMCID: PMC10986006
PMID: 38561866
Abstract
Huntington's disease (HD) is a devastating neurodegenerative disorder caused by aggregation of the mutant huntingtin (mHTT) protein, resulting from a CAG repeat expansion in the huntingtin gene HTT. HD is characterized by a variety of debilitating symptoms including involuntary movements, cognitive impairment, and psychiatric disturbances. Despite considerable efforts, effective disease-modifying treatments for HD remain elusive, necessitating exploration of novel therapeutic approaches, including lifestyle modifications that could delay symptom onset and disease progression. Recent studies suggest that time-restricted eating (TRE), a form of intermittent fasting involving daily caloric intake within a limited time window, may hold promise in the treatment of neurodegenerative diseases, including HD. TRE has been shown to improve mitochondrial function, upregulate autophagy, reduce oxidative stress, regulate the sleep-wake cycle, and enhance cognitive function. In this review, we explore the potential therapeutic role of TRE in HD, focusing on its underlying physiological mechanisms. We discuss how TRE might enhance the clearance of mHTT, recover striatal brain-derived neurotrophic factor levels, improve mitochondrial function and stress-response pathways, and synchronize circadian rhythm activity. Understanding these mechanisms is critical for the development of targeted lifestyle interventions to mitigate HD pathology and improve patient outcomes. While the potential benefits of TRE in HD animal models are encouraging, future comprehensive clinical trials will be necessary to evaluate its safety, feasibility, and efficacy in persons with HD.
Details
- Title: Subtitle
- Dietary fasting and time-restricted eating in Huntington's disease: therapeutic potential and underlying mechanisms
- Creators
- Russell G Wells - Oregon Health & Science UniversityLee E Neilson - Oregon Health & Science UniversityAndrew W McHill - Oregon Health & Science UniversityAmie L Hiller - VA Portland Health Care System
- Resource Type
- Journal article
- Publication Details
- Translational neurodegeneration, Vol.13(1), pp.17-13
- DOI
- 10.1186/s40035-024-00406-z
- PMID
- 38561866
- PMCID
- PMC10986006
- NLM abbreviation
- Transl Neurodegener
- ISSN
- 2047-9158
- eISSN
- 2047-9158
- Grant note
- I01 CX000253 / CSRD VA IK2 CX002539 / CSRD VA
- Language
- English
- Date published
- 04/02/2024
- Academic Unit
- Neurology
- Record Identifier
- 9985089434902771
Metrics
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