Evidence map›Paper›PMID 30918302›Full record

ArticleScientific reports2019

Stimulation of noradrenergic transmission by reboxetine is beneficial for a mouse model of progressive parkinsonism.

Grzegorz Kreiner, Katarzyna Rafa-Zabłocka, Justyna Barut, Piotr Chmielarz, Marta Kot, Monika Bagińska, Rosanna Parlato, Władysława Anna Daniel, Irena Nalepa

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

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  14. The Noradrenergic System in Parkinson's Disease.Frontiers in pharmacology · 2020
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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

9 authors at 2 institutions in 2 countries.

Grzegorz KreinerDepartment Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, 31-343, Kraków, Smętna 12, Poland. kreiner@if-pan.krakow.pl.
Katarzyna Rafa-ZabłockaDepartment Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, 31-343, Kraków, Smętna 12, Poland.ORCID http://orcid.org/0000-0001-9622-3476
Justyna BarutDepartment Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, 31-343, Kraków, Smętna 12, Poland.
Piotr ChmielarzDepartment Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, 31-343, Kraków, Smętna 12, Poland.
Marta KotDepartment Pharmacokinetics and Drug Metabolism, Institute of Pharmacology, Polish Academy of Sciences, 31-343, Kraków, Smętna 12, Poland.
Monika BagińskaDepartment Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, 31-343, Kraków, Smętna 12, Poland.
Rosanna ParlatoInstitute of Applied Physiology, University of Ulm, 89081, Ulm, Germany.
Władysława Anna DanielDepartment Pharmacokinetics and Drug Metabolism, Institute of Pharmacology, Polish Academy of Sciences, 31-343, Kraków, Smętna 12, Poland.
Irena NalepaDepartment Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, 31-343, Kraków, Smętna 12, Poland.
Maj Institute of Pharmacology · PLUniversität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is the second most common neurodegenerative disorder and is characterized by motor deficits such as tremor, rigidity and bradykinesia. These symptoms are directly caused by the loss of dopaminergic neurons. However, a wealth of clinical evidence indicates that the dopaminergic system is not the only system affected in PD. Postmortem studies of brains from PD patients have revealed the degeneration of noradrenergic neurons in the locus coeruleus (LC) to the same or even greater extent than that observed in the dopaminergic neurons of substantia nigra (SN) and ventral tegmental area (VTA). Moreover, studies performed on rodent models suggest that enhancement of noradrenergic transmission may attenuate the PD-like phenotype induced by MPTP administration, a neurotoxin-based PD model. The aim of this study was to investigate whether chronic treatment with either of two compounds targeting the noradrenergic system (reboxetine or atipamezole) possess the ability to reduce the progression of a PD-like phenotype in a novel mouse model of progressive dopaminergic neurodegeneration induced by the genetic inhibition of rRNA synthesis in dopaminergic neurons, mimicking a PD-like phenotype. The results showed that reboxetine improved the parkinsonian phenotype associated with delayed progression of SN/VTA dopaminergic neurodegeneration and higher dopamine content in the striatum. Moreover, the alpha1-adrenergic agonist phenylephrine enhanced survival of TH+ neurons in primary cell cultures, supporting the putative neuroprotective effects of noradrenergic stimulation. Our results provide new insights regarding the possible influence of the noradrenergic system on dopaminergic neuron survival and strongly support the hypothesis regarding the neuroprotective role of noradrenaline.

Indexed as

AnimalsCells, CulturedChromatography, High Pressure LiquidDisease Models, AnimalDopaminergic NeuronsFemaleImidazolesImmunohistochemistryLocus CoeruleusMaleMiceMice, Inbred C57BLParkinsonian DisordersReboxetineSubstantia NigraVentral Tegmental AreaatipamezoleImidazolesReboxetine

Identifiers

PMID30918302
PMCPMC6437187
OpenAlexW2922564535

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Registered trials

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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.