Evidence map›Paper›PMID 31276792›Full record

ArticleNeurobiology of disease2019

Time course and magnitude of alpha-synuclein inclusion formation and nigrostriatal degeneration in the rat model of synucleinopathy triggered by intrastriatal α-synuclein preformed fibrils.

Joseph R Patterson, Megan F Duffy, Christopher J Kemp, Jacob W Howe, Timothy J Collier, Anna C Stoll, Kathryn M Miller, Pooja Patel, Nathan Levine, Darren J Moore and 6 more

Abstract read
In one paragraph

Article in Neurobiology of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing 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

61 citing papers in PubMed.

  1. Review
  2. Article
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  4. A novel rat model of body first subtype of Parkinson's disease.bioRxiv : the preprint server for biology · 2026
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  6. Shared Epitope-PositiveNeurology(R) neuroimmunology & neuroinflammation · 2026
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  11. Review
  12. Disease-modifying, multidimensional efficacy of putaminal CaMolecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
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  15. Review
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  17. Review
  18. The raphe nuclei are the early lesion site of gastricActa pharmaceutica Sinica. B · 2024
    Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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

16 authors.

Joseph R PattersonDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA. Electronic address: Joseph.Patterson@hc.msu.edu.
Megan F DuffyDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA; Neuroscience Program, Michigan State University, East Lansing, MI, USA.
Christopher J KempDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA.
Jacob W HoweDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA.
Timothy J CollierDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA; Neuroscience Program, Michigan State University, East Lansing, MI, USA; Mercy Health Hauenstein Neuroscience Medical Center, Grand Rapids, MI, USA.
Anna C StollDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA; Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI, USA.
Kathryn M MillerDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA; Neuroscience Program, Michigan State University, East Lansing, MI, USA.
Pooja PatelDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA.
Nathan LevineCenter of Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI, USA.
Darren J MooreCenter of Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI, USA.
Kelvin C LukCenter for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA.
Sheila M FlemingCollege of Pharmacy, Northeast Ohio Medical University, Rootstown, OH, USA.
Nicholas M KanaanDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA; Neuroscience Program, Michigan State University, East Lansing, MI, USA; Mercy Health Hauenstein Neuroscience Medical Center, Grand Rapids, MI, USA.
Katrina L PaumierDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA.
Omar M A El-AgnafNeurological Disorders Researcher Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation, Doha, Qatar.
Caryl E SortwellDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA; Neuroscience Program, Michigan State University, East Lansing, MI, USA; Mercy Health Hauenstein Neuroscience Medical Center, Grand Rapids, MI, USA.

Funding

Integrative Training in the Pharmacological SciencesT32GM092715 · NIGMS · MICHIGAN STATE UNIVERSITY · PI NEUBIG, RICHARD R · 2011 to 2020
$1.5M
The Rat Pre-Formed Alpha-Synuclein Fibril Model of Parkinson's DiseaseR21NS099416 · NINDS · MICHIGAN STATE UNIVERSITY · PI SORTWELL, CARYL E · 2017 to 2017
$398k
NIGMS NIH HHS T32 GM092715NINDS NIH HHS R21 NS099416
6 · The paper itself

Abstract

Animal models that accurately recapitulate the accumulation of alpha-synuclein (α-syn) inclusions, progressive neurodegeneration of the nigrostriatal system and motor deficits can be useful tools for Parkinson's disease (PD) research. The preformed fibril (PFF) synucleinopathy model in rodents generally displays these PD-relevant features, however, the magnitude and predictability of these events is far from established. We therefore sought to optimize the magnitude of α-syn accumulation and nigrostriatal degeneration, and to understand the time course of both. Rats were injected unilaterally with different quantities of α-syn PFFs (8 or 16 μg of total protein) into striatal sites selected to concentrate α-syn inclusion formation in the substantia nigra pars compacta (SNpc). Rats displayed an α-syn PFF quantity-dependent increase in the magnitude of ipsilateral SNpc inclusion formation at 2 months and bilateral loss of nigral dopamine neurons at 6 months. Unilateral 16 μg PFF injection also resulted in modest sensorimotor deficits in forelimb adjusting steps associated with degeneration at 6 months. Bilateral injection of 16 μg α-syn PFFs resulted in symmetric bilateral degeneration equivalent to the ipsilateral nigral degeneration observed following unilateral 16 μg PFF injection (~50% loss). Bilateral PFF injections additionally resulted in alterations in several gait analysis parameters. These α-syn PFF parameters can be applied to generate a reproducible synucleinopathy model in rats with which to study pathogenic mechanisms and vet potential disease-modifying therapies.

Indexed as

alpha-SynucleinAnimalsCorpus StriatumDisease Models, AnimalDopaminergic NeuronsInclusion BodiesMaleRatsRats, Inbred F344Substantia NigraSynucleinopathiesalpha-SynucleinAlpha-SynucleinParkinson's diseasePreformed fibrilsSynucleinopathy

Identifiers

PMID31276792
PMCPMC6701176

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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.