Evidence map›Paper›PMID 23353924›Full record

ReviewExperimental neurology2013

Circadian dysfunction may be a key component of the non-motor symptoms of Parkinson's disease: insights from a transgenic mouse model.

L David Willison, Takashi Kudo, Dawn H Loh, Dika Kuljis, Christopher S Colwell

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.3field-weighted citation impact, top 8% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 75 citations in OpenAlex.

  1. Circadian Neurology.Continuum (Minneapolis, Minn.) · 2026
    Review
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  15. Disturbances of Sleep and Alertness in Parkinson's Disease.Current neurology and neuroscience reports · 2018
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Sleep and clocks - implications for brain health.Neurobiology of sleep and circadian rhythms · 2017
    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

5 authors at 1 institution in 1 country.

L David WillisonDivision of Child and Adolescent Psychiatry, Laboratory of Circadian and Sleep Medicine, University of California, Los Angeles, David Geffen School of Medicine, Los Angeles, CA, USA.
Takashi Kudo
Dawn H Loh
Dika Kuljis
Christopher S Colwell
University of California, Los Angeles · US

Funding

Neuroendocrinology, Sex Differences, and ReproductionT32HD007228 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARNOLD, ARTHUR P · 1985 to 2015
$3.9M
NICHD NIH HHS T32 HD007228
6 · The paper itself

Abstract

Sleep disorders are nearly ubiquitous among patients with Parkinson's disease (PD), and they manifest early in the disease process. While there are a number of possible mechanisms underlying these sleep disturbances, a primary dysfunction of the circadian system should be considered as a contributing factor. Our laboratory's behavioral phenotyping of a well-validated transgenic mouse model of PD reveals that the electrical activity of neurons within the master pacemaker of the circadian system, the suprachiasmatic nuclei (SCN), is already disrupted at the onset of motor symptoms, although the core features of the intrinsic molecular oscillations in the SCN remain functional. Our observations suggest that the fundamental circadian deficit in these mice lies in the signaling output from the SCN, which may be caused by known mechanisms in PD etiology: oxidative stress and mitochondrial disruption. Disruption of the circadian system is expected to have pervasive effects throughout the body and may itself lead to neurological and cardiovascular disorders. In fact, there is much overlap in the non-motor symptoms experienced by PD patients and in the consequences of circadian disruption. This raises the possibility that the sleep and circadian dysfunction experienced by PD patients may not merely be a subsidiary of the motor symptoms, but an integral part of the disease. Furthermore, we speculate that circadian dysfunction can even accelerate the pathology underlying PD. If these hypotheses are correct, more aggressive treatment of the circadian misalignment and sleep disruptions in PD patients early in the pathogenesis of the disease may be powerful positive modulators of disease progression and patient quality of life.

Indexed as

Disease Models, AnimalAnimalsCircadian RhythmHumansMiceMice, TransgenicOxidative StressParkinson DiseaseSleep Wake DisordersSuprachiasmatic Nucleus

Identifiers

PMID23353924
PMCPMC3994881
OpenAlexW2080688766

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.