Evidence map›Paper›PMID 29865270›Full record

ArticleInternational journal of molecular sciences2018

Impaired Photic Entrainment of Spontaneous Locomotor Activity in Mice Overexpressing Human Mutant α-Synuclein.

Martina Pfeffer, Zuzana Zimmermann, Suzana Gispert, Georg Auburger, Horst-Werner Korf, Charlotte von Gall

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  12. The Effects of Light and the Circadian System on Rhythmic Brain Function.International journal of molecular sciences · 2022
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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

6 authors at 2 institutions in 1 country.

Martina PfefferInstitut für Anatomie II, Fachbereich Medizin, Heinrich Heine Universität, Universitätsstr. 1, D-40225 Düsseldorf, Germany. Martina.Pfeffer@med.uni-duesseldorf.de.
Zuzana ZimmermannDr. Senckenbergische Anatomie II, Fachbereich Medizin, Goethe-Universität Frankfurt, Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany. Zuzana.Zimmermann@gmx.de.
Suzana GispertExperimental Neurology, Department of Neurology, Goethe-Universität Frankfurt, Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany. Gispert-sanchez@em.uni-frankfurt.de.
Georg AuburgerExperimental Neurology, Department of Neurology, Goethe-Universität Frankfurt, Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany. Auburger@em.uni-frankfurt.de.
Horst-Werner KorfInstitut für Anatomie I, Fachbereich Medizin, Heinrich Heine Universität, Universitätsstr. 1, D-40225 Düsseldorf, Germany. Korf@uni-duesseldorf.de.
Charlotte von GallInstitut für Anatomie II, Fachbereich Medizin, Heinrich Heine Universität, Universitätsstr. 1, D-40225 Düsseldorf, Germany. Charlotte.Gall@med.uni-duesseldorf.de.
Goethe University Frankfurt · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is characterized by distinct motor and non-motor symptoms. Sleep disorders are the most frequent and challenging non-motor symptoms in PD patients, and there is growing evidence that they are a consequence of disruptions within the circadian system. PD is characterized by a progressive degeneration of the dorsal vagal nucleus and midbrain dopaminergic neurons together with an imbalance of many other neurotransmitters. Mutations in α-synuclein (SNCA), a protein modulating SNARE complex-dependent neurotransmission, trigger dominantly inherited PD variants and sporadic cases of PD. The A53T SNCA missense mutation is associated with an autosomal dominant early-onset familial PD. To test whether this missense mutation affects the circadian system, we analyzed the spontaneous locomotor behavior of non-transgenic wildtype mice and transgenic mice overexpressing mutant human A53T α-synuclein (A53T). The mice were subjected to entrained- and free-running conditions as well as to experimental jet lag. Furthermore, the vesicular glutamate transporter 2 (VGLUT2) in the suprachiasmatic nucleus (SCN) was analyzed by immunohistochemistry. Free-running circadian rhythm and, thus, circadian rhythm generation, were not affected in A53T mice. A53T mice entrained to the light⁻dark cycle, however, with an advanced phase angle of 2.65 ± 0.5 h before lights off. Moreover, re-entrainment after experimental jet lag was impaired in A53T mice. Finally, VGLUT2 immunoreaction was reduced in the SCN of A53T mice. These data suggest an impaired light entrainment of the circadian system in A53T mice.

Indexed as

Circadian ClocksDisease Models, AnimalLocomotionSynaptic Transmissionalpha-SynucleinAnimalsGene Expression RegulationMiceMice, TransgenicMutationParkinson DiseasePhotic StimulationUp-Regulationalpha-SynucleinSNCA protein, humanactographycircadian rhythmsendogenous clockParkinson diseasevesicular glutamate transporter 2

Identifiers

PMID29865270
PMCPMC6032049
OpenAlexW2806084688

What OpenQuestion holds

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LicenceCC BY
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.