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Dietary fasting and time-restricted eating in Huntington's disease: therapeutic potential and underlying mechanisms

Russell G Wells1, Lee E Neilson2,3, Andrew W McHill4,5

  • 1Department of Neurology, Oregon Health and Science University, 3181 SW Sam Jackson Park Rd, Portland, OR, 97239, USA. wellsru@ohsu.edu.

Translational Neurodegeneration
|April 2, 2024
PubMed

Insights

Time-restricted eating (TRE), a form of intermittent fasting, may offer a novel therapeutic strategy for Huntington's disease (HD). This lifestyle intervention shows potential for clearing toxic proteins and improving cellular functions implicated in HD progression.

Area of Science:

  • Neuroscience
  • Genetics
  • Metabolic Disorders

Background:

  • Huntington's disease (HD) is a fatal neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin gene, leading to mutant huntingtin (mHTT) protein aggregation.
  • Current treatments for HD are largely symptomatic, highlighting the urgent need for disease-modifying therapies and lifestyle interventions.
  • Time-restricted eating (TRE), a dietary approach involving a daily eating window, has emerged as a potential intervention for neurodegenerative conditions.

Purpose of the Study:

  • To explore the potential therapeutic role of time-restricted eating (TRE) in managing Huntington's disease (HD).
  • To elucidate the underlying physiological mechanisms by which TRE may mitigate HD pathology.
  • To assess the feasibility of TRE as a lifestyle intervention for individuals with HD.

Main Methods:

  • Review of existing scientific literature on TRE and its effects on cellular pathways relevant to neurodegeneration.
  • Analysis of proposed mechanisms by which TRE could impact mHTT clearance, mitochondrial function, and circadian rhythms in the context of HD.
  • Examination of preclinical data suggesting TRE's benefits in HD models.

Main Results:

  • TRE demonstrates potential to improve mitochondrial function, enhance autophagy, and reduce oxidative stress, all critical factors in HD pathogenesis.
  • TRE may facilitate the clearance of mutant huntingtin (mHTT) protein aggregates.
  • The intervention could restore striatal brain-derived neurotrophic factor (BDNF) levels and synchronize circadian rhythms, potentially alleviating HD symptoms.

Conclusions:

  • Time-restricted eating (TRE) presents a promising, non-pharmacological approach to potentially slow Huntington's disease progression.
  • Understanding TRE's impact on mHTT clearance, cellular stress, and circadian rhythms is key to developing effective lifestyle interventions for HD.
  • Further clinical trials are essential to validate the safety and efficacy of TRE in human patients with Huntington's disease.

Keywords:
AutophagyCircadian rhythmDietary fastingHuntington’s diseaseIntermittent fastingLifestyle interventionMitochondrial biogenesisNeuroprotectionTime-restricted eating

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