Evidence map›Paper›PMID 29302618›Full record

ArticleeNeuro

Time-Restricted Feeding Improves Circadian Dysfunction as well as Motor Symptoms in the Q175 Mouse Model of Huntington's Disease.

Huei-Bin Wang, Dawn H Loh, Daniel S Whittaker, Tamara Cutler, David Howland, Christopher S Colwell

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03439618 (Comparison of Time-restricted Feeding and Continuous Feeding in Critically Ill Patients), which is not on this map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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.

NCT03439618 naunknown statusnot on this map

Comparison of Time-restricted Feeding and Continuous Feeding in Critically Ill Patients

TypeinterventionalSponsorQingdao UniversityRan2018 to 2022Enrolled380ConditionsFeeding BehaviorArmstime-restricted feeding, continuous feeding
3 · Its place in the literature

Who cites it

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Timing the decline: Cellular circadian rhythms and Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article
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

6 authors at 2 institutions in 1 country.

Huei-Bin WangDepartment of Psychiatry and Biobehavioral Sciences, University of California - Los Angeles, Los Angeles, CA 90024-1759.
Dawn H LohDepartment of Psychiatry and Biobehavioral Sciences, University of California - Los Angeles, Los Angeles, CA 90024-1759.
Daniel S WhittakerDepartment of Psychiatry and Biobehavioral Sciences, University of California - Los Angeles, Los Angeles, CA 90024-1759.ORCID 0000-0002-4293-5192
Tamara CutlerDepartment of Psychiatry and Biobehavioral Sciences, University of California - Los Angeles, Los Angeles, CA 90024-1759.
David HowlandCHDI Foundation, Princeton, NJ 08540.
Christopher S ColwellDepartment of Psychiatry and Biobehavioral Sciences, University of California - Los Angeles, Los Angeles, CA 90024-1759.ORCID 0000-0002-1059-184X
University of California, Los Angeles · USCHDI Foundation · US

Funding

UCLA Center for Translational Research in Neurodevelopment: UC-TRaNU54HD087101 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MCCRACKEN, JAMES T. · 2016 to 2020
$6.5M
NICHD NIH HHS U54 HD087101
6 · The paper itself

Abstract

Huntington's disease (HD) patients suffer from a progressive neurodegeneration that results in cognitive, psychiatric, cardiovascular, and motor dysfunction. Disturbances in sleep/wake cycles are common among HD patients with reports of delayed sleep onset, frequent bedtime awakenings, and fatigue during the day. The heterozygous Q175 mouse model of HD has been shown to phenocopy many HD core symptoms including circadian dysfunctions. Because circadian dysfunction manifests early in the disease in both patients and mouse models, we sought to determine if early intervention that improve circadian rhythmicity can benefit HD and delay disease progression. We determined the effects of time-restricted feeding (TRF) on the Q175 mouse model. At six months of age, the animals were divided into two groups: ad libitum (ad lib) and TRF. The TRF-treated Q175 mice were exposed to a 6-h feeding/18-h fasting regimen that was designed to be aligned with the middle of the time when mice are normally active. After three months of treatment (when mice reached the early disease stage), the TRF-treated Q175 mice showed improvements in their locomotor activity rhythm and sleep awakening time. Furthermore, we found improved heart rate variability (HRV), suggesting that their autonomic nervous system dysfunction was improved. Importantly, treated Q175 mice exhibited improved motor performance compared to untreated Q175 controls, and the motor improvements were correlated with improved circadian output. Finally, we found that the expression of several HD-relevant markers was restored to WT levels in the striatum of the treated mice using NanoString gene expression assays.

Indexed as

Circadian RhythmMotor ActivityAnimalsAutonomic Nervous SystemDisease Models, AnimalEatingFastingHeart RateHuntington DiseaseMaleMice, Inbred C57BLMice, TransgenicSleepTime Factorscircadian rhythmsfast/feed cycleHuntington’s diseaseQ175time-restricted feeding

Identifiers

PMID29302618
PMCPMC5752678
OpenAlexW2782399764

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.