Evidence map›Paper›PMID 38374883›Full record

ArticleFrontiers in aging neuroscience2024

Nigral transcriptomic profiles in Engrailed-1 hemizygous mouse models of Parkinson's disease reveal upregulation of oxidative phosphorylation-related genes associated with delayed dopaminergic neurodegeneration.

Lautaro Francisco Belfiori, Alfredo Dueñas Rey, Dorottya Mária Ralbovszki, Itzia Jimenez-Ferrer, Filip Fredlund, Sagar Shivayogi Balikai, Dag Ahrén, Kajsa Atterling Brolin, Maria Swanberg

Abstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

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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

2 citing papers in PubMed.

  1. Review
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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Lautaro Francisco Belfiori *Translational Neurogenetics Unit, Wallenberg Neuroscience Center, Department of Experimental Medical Sciences, Lund University, Lund, Sweden.
Alfredo Dueñas Rey *Translational Neurogenetics Unit, Wallenberg Neuroscience Center, Department of Experimental Medical Sciences, Lund University, Lund, Sweden.
Dorottya Mária RalbovszkiTranslational Neurogenetics Unit, Wallenberg Neuroscience Center, Department of Experimental Medical Sciences, Lund University, Lund, Sweden.
Itzia Jimenez-FerrerTranslational Neurogenetics Unit, Wallenberg Neuroscience Center, Department of Experimental Medical Sciences, Lund University, Lund, Sweden.
Filip FredlundTranslational Neurogenetics Unit, Wallenberg Neuroscience Center, Department of Experimental Medical Sciences, Lund University, Lund, Sweden.
Sagar Shivayogi BalikaiTranslational Neurogenetics Unit, Wallenberg Neuroscience Center, Department of Experimental Medical Sciences, Lund University, Lund, Sweden.
Dag AhrénDepartment of Biology, National Bioinformatics Infrastructure Sweden (NBIS), SciLifeLab, Stockholm, Sweden.
Kajsa Atterling BrolinTranslational Neurogenetics Unit, Wallenberg Neuroscience Center, Department of Experimental Medical Sciences, Lund University, Lund, Sweden.
Maria SwanbergTranslational Neurogenetics Unit, Wallenberg Neuroscience Center, Department of Experimental Medical Sciences, Lund University, Lund, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Parkinson's disease (PD) is the second most common neurodegenerative disorder, increasing both in terms of prevalence and incidence. To date, only symptomatic treatment is available, highlighting the need to increase knowledge on disease etiology in order to develop new therapeutic strategies. Hemizygosity for the gene Engrailed-1 ( Methods: Transcriptome profiles were defined by RNAseq in microdissected substantia nigra from 1-week old OF1, OF1- Results: Nigrostriatal neurodegeneration was manifested in OF1- Discussion: Our results suggest that increased expression of genes encoding mitochondrial proteins before the onset of neurodegeneration is associated with increased resistance to PD-like nigrostriatal neurodegeneration. This highlights the importance of genetic background in PD models, how different strains can be used to model clinical and sub-clinical pathologies and provides insights to gene expression mechanisms associated with PD susceptibility and progression.

Indexed as

genetic susceptibilitymitochondrianeurodegenerationParkinson’s diseasesubstantia nigratranscriptomics

Identifiers

PMID38374883
PMCPMC10875038

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