Evidence map›Paper›PMID 27046648›Full record

ArticleMolecular psychiatry2017

Circadian rhythm dysfunction: a novel environmental risk factor for Parkinson's disease.

E Lauretti, A Di Meco, S Merali, D Praticò

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
7.2field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 110 citations in OpenAlex.

  1. Circadian clock communication during homeostasis and ageing.Nature reviews. Molecular cell biology · 2025
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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.

E LaurettiDepartment of Pharmacology, Center for Translational Medicine, School of Medicine, Temple University, Philadelphia, PA, USA.
A Di MecoDepartment of Pharmacology, Center for Translational Medicine, School of Medicine, Temple University, Philadelphia, PA, USA.
S MeraliDepartment of Pharmaceutical Sciences, School of Pharmacy, Temple University, Philadelphia, PA, USA.
D PraticòDepartment of Pharmacology, Center for Translational Medicine, School of Medicine, Temple University, Philadelphia, PA, USA.
Temple University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a chronic and progressive neurodegenerative disorder. Although rare genetically linked cases of PD have been reported, most incidences are sporadic in nature. Late-onset, sporadic PD is thought to result from the combined effects of genetic and environmental risk factors exposure. Sleep and circadian rhythm disorders are recurrent among PD patients and appear early in the disease. Although some evidence supports a relationship between circadian disruption (CD) and PD, whether this is secondary to the motor symptoms or, indeed, is a factor that contributes to the pathogenesis of the disease remains to be investigated. In the present paper, we studied the direct consequence of chronic CD on the development of the phenotype in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinen) model of PD. Pre-exposure to CD to mice treated with MPTP resulted in an exacerbation of motor deficit and a significant reduction in the capability of acquiring motor skills. These changes were associated with a greater loss of tyrosine hydroxylase cell content and intense neuroinflammation. Taken together, our findings demonstrate that CD by triggering a robust neuroinflammatory reaction and degeneration of the nigral-dopaminergic neuronal system exacerbates motor deficit. They support the novel hypothesis that circadian rhythm disorder is an environmental risk factor for developing PD.

Indexed as

AnimalsBehavior, AnimalChronobiology DisordersCircadian RhythmDisease Models, AnimalDopaminergic NeuronsMaleMiceMice, Inbred C57BLMotor ActivityNerve DegenerationNeuroprotective AgentsParkinson DiseaseRisk FactorsTyrosine 3-MonooxygenaseNeuroprotective AgentsTyrosine 3-Monooxygenase

Identifiers

PMID27046648
OpenAlexW2313741717

What OpenQuestion holds

Textmetadata
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.