Evidence map›Paper›PMID 38351057›Full record

ArticleeNeuro2024

Mice Expressing A53T/A30P Mutant Alpha-Synuclein in Dopamine Neurons Do Not Display Behavioral Deficits.

Cameron Keomanivong, Josephine Schamp, Ervina Tabakovic, Ramasamy Thangavel, Georgina Aldridge, Andrew A Pieper, Nandakumar S Narayanan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eNeuro, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 43% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

7 authors at 3 institutions in 3 countries.

Cameron KeomanivongCarver College of Medicine, University of Iowa, Iowa City 52245, Iowa.
Josephine SchampYork University, York 68467, Nebraska.
Ervina TabakovicCarver College of Medicine, University of Iowa, Iowa City 52245, Iowa.
Ramasamy ThangavelDepartment of Neurology, University of Iowa, Iowa City 52245, Iowa.
Georgina AldridgeDepartment of Neurology, University of Iowa, Iowa City 52245, Iowa.
Andrew A PieperBrain Health Medicines Center, Harrington Discovery Institute, University Hospitals Cleveland Medical Center, Cleveland 44106, Ohio; Department of Psychiatry, Case Western Reserve University, Cleveland 44106, Ohio; Geriatric Research Education and Clinical Center (GRECC), Louis Stokes Cleveland VA Medical Center, Cleveland 44106, Ohio; Institute for Transformative Molecular Medicine, School of Medicine, Case Western Reserve University, Cleveland 44106, Ohio; Department of Pathology, School of Medicine, Case Western Reserve University, Cleveland 44106, Ohio; Department of Neuroscience, School of Medicine, Case Western Reserve University, Cleveland 44106, Ohio; Translational Therapeutics Core, Cleveland Alzheimer's Disease Research Center, Cleveland, Ohio.
Nandakumar S NarayananDepartment of Neurology, University of Iowa, Iowa City 52245, Iowa nandakumar-narayanan@uiowa.edu.ORCID https://orcid.org/0000-0002-0427-0003
University of Iowa · USUniversity Hospitals of Cleveland · USYork University · CA

Funding

VTA dopamine neurons and cognitive symptoms of Parkinson’s diseaseR01NS120987 · NINDS · UNIVERSITY OF IOWA · PI NARAYANAN, NANDAKUMAR · 2021 to 2025
$2.0M
Medical Student Summer Research ProgramT35HL166206 · NHLBI · UNIVERSITY OF IOWA · PI ROBERT D ROGHAIR · 2023 to 2026
$598k
NHLBI NIH HHS T35 HL166206NINDS NIH HHS R01 NS120987
6 · The paper itself

Abstract

Alpha-synuclein has been implicated in neurodegenerative diseases such as Parkinson's disease and dementia with Lewy bodies, with A53T and A30P mutations shown to be disease causing. It has been reported that hemizygous transgenic mice with tyrosine hydroxylase promotor-driven expression of A53T/A30P mutant alpha-synuclein in dopamine neurons provide a useful preclinical model of these conditions by virtue of developing behavioral deficits. Here, we report a lack of replication of this finding. Despite detecting robust overexpression of A53T/A30P mutant alpha-synuclein in dopamine neurons, we did not observe decreased tyrosine hydroxylase immunofluorescence or behavioral deficits in these mice. Our results demonstrate that preclinical models of synucleinopathy need careful validation in the field.

Indexed as

alpha-SynucleinParkinson DiseaseAnimalsDisease Models, AnimalDopaminergic NeuronsMiceMice, TransgenicTyrosine 3-Monooxygenasealpha-SynucleinSnca protein, mouseTyrosine 3-Monooxygenaseanimal modelsbehaviordopaminemidbrainreplication

Identifiers

PMID38351057
PMCPMC10866330
OpenAlexW4391773618

What OpenQuestion holds

Textmetadata
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.