Evidence map›Paper›PMID 38561866›Full record

ReviewTranslational neurodegeneration2024

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

Russell G Wells, Lee E Neilson, Andrew W McHill, Amie L Hiller

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Translational neurodegeneration, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06490367 (Safety, Feasibility, and Biomarker Effects of Time-restricted Eating for 12 Weeks in Early-stage Huntington's Disease.), which is not on this map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT06490367 nacompletednot on this map

Safety, Feasibility, and Biomarker Effects of Time-restricted Eating for 12 Weeks in Early-stage Huntington's Disease.

TypeinterventionalSponsorOregon Health and Science UniversityRan2024 to 2025Enrolled22ConditionsHuntington DiseaseArmsTime-Restricted Eating Diet
3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

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  20. Caveolae with serotonin and NMDA receptors as promising targets for the treatment of Alzheimer's disease.International journal of physiology, pathophysiology and pharmacology · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Russell G WellsDepartment of Neurology, Oregon Health and Science University, 3181 SW Sam Jackson Park Rd, Portland, OR, 97239, USA. wellsru@ohsu.edu.ORCID 0000-0001-6534-7863
Lee E NeilsonDepartment of Neurology, Oregon Health and Science University, 3181 SW Sam Jackson Park Rd, Portland, OR, 97239, USA.
Andrew W McHillSleep, Chronobiology and Health Laboratory, School of Nursing, Oregon Health & Science University, Portland, OR, 97239, USA.
Amie L HillerDepartment of Neurology, Oregon Health and Science University, 3181 SW Sam Jackson Park Rd, Portland, OR, 97239, USA.
Oregon Health & Science University · US

Funding

Neurobiology of Suicide Risk in Traumatic Brain Injury and Substance AbuseI01CX000253 · VA · VA SALT LAKE CITY HEALTHCARE SYSTEM · PI YURGELUN-TODD, DEBORAH A. · 2009 to 2013
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Biomarkers of disease severity and progression in Parkinson'sIK2CX002539 · VA · PORTLAND VA MEDICAL CENTER · PI Lee Neilson · 2023 to 2026
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CSRD VA I01 CX000253CSRD VA IK2 CX002539
6 · The paper itself

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.

Indexed as

Huntington DiseaseNeurodegenerative DiseasesAnimalsFastingHumansOxidative StressAutophagyCircadian rhythmDietary fastingHuntington’s diseaseIntermittent fastingLifestyle interventionMitochondrial biogenesisNeuroprotectionTime-restricted eating

Identifiers

PMID38561866
PMCPMC10986006
OpenAlexW4393443267

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.