Evidence map›Paper›PMID 41554867›Full record

ArticleScientific reports2026

Characterization of motor and non-motor features associated with bilateral nigral degeneration due to A53T alpha-synuclein in female rats.

Laura Kondrataviciute, Minesh Kapadia, Hien Chau, Cherisse Tan, Polly Ou, Ritisha Mukherjee, Sarah Hui, Sabika Jafri, Jimmy George, Ivan Skelin and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. 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
–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

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. 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

14 authors.

Laura KondrataviciuteInstitute of Biomedical Engineering, University of Toronto, Toronto, Canada.
Minesh KapadiaKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, Canada.
Hien ChauKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, Canada.
Cherisse TanLaboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada.
Polly OuLaboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada.
Ritisha MukherjeeNeuroscience and Pharmacology, University of Toronto, Toronto, Canada.
Sarah HuiKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, Canada.
Sabika JafriKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, Canada.
Jimmy GeorgeKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, Canada.
Ivan SkelinKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, Canada.
Taufik ValianteInstitute of Biomedical Engineering, University of Toronto, Toronto, Canada.
Luka MilosevicInstitute of Biomedical Engineering, University of Toronto, Toronto, Canada.
Lorraine V KaliaKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, Canada. Lorraine.kalia@uhn.ca.
Suneil K KaliaKrembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, Canada. Suneil.Kalia@uhn.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is characterized by the loss of dopaminergic neurons in the substantia nigra (SN), accumulation of alpha-synuclein (a-Syn)-rich aggregates, and the development of both motor and non-motor symptoms. The absence of a cure for PD underscores the critical need for animal models that recapitulate both its molecular hallmarks and the spectrum of behavioral symptoms to elucidate pathogenic mechanisms and advance therapeutic development. While the virus-mediated a-Syn overexpression rat model recapitulates progressive dopaminergic neurodegeneration and motor deficits, its non-motor phenotypic profile remains poorly characterized. In this study, we investigated the behavioral consequences of targeted adeno-associated virus (AAV)-mediated overexpression of aggregate-prone mutant A53T a-Syn within the rat SN bilaterally. We confirmed dopaminergic neurodegeneration within 6 weeks, along with progressive motor impairments evident as reduced locomotion in the open field test and increased foot slips in the grid walking test as early as 3 weeks post-AAV injection. The dopaminergic origin of the motor deficit in the grid walking was confirmed at the 6-week timepoint by its attenuation with L-DOPA treatment. Crucially, animals overexpressing A53T a-Syn exhibited reduced responsiveness to palatable stimulation in the sucrose preference test in the context of advanced neurodegeneration. No changes in anxiety-like behaviors, olfactory function, or recognition memory were observed when compared with age-matched controls. These findings suggest that, in addition to motor impairments, bilateral A53T a-Syn overexpression induces depression-like behavior, providing a valuable tool for studying the pathogenesis and treatment of non-motor affective symptoms in PD.

Indexed as

alpha-SynucleinParkinson DiseaseSubstantia NigraAnimalsBehavior, AnimalDependovirusDisease Models, AnimalDopaminergic NeuronsFemaleMotor ActivityRatsalpha-SynucleinAlpha-synucleinDepressionMotor behaviorNon-motor behaviorParkinson’s diseaseRat Model

Identifiers

PMID41554867
PMCPMC12886899

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.