Evidence map›Paper›PMID 22753348›Full record

ReviewMovement disorders : official journal of the Movement Disorder Society2013

Animal models of Parkinson's disease: limits and relevance to neuroprotection studies.

Erwan Bezard, Zhenyu Yue, Deniz Kirik, Maria Grazia Spillantini

Registry-linked trialAbstract readReview
In one paragraph

Review in Movement disorders : official journal of the Movement Disorder Society, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03329833 (Motivational Interviewing and Physical Activity Change in Parkinson's Disease), which is not on this map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing 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.

NCT03329833 naunknown statusnot on this mapstarted 2017, after this paper: background citation

Motivational Interviewing and Physical Activity Change in Parkinson's Disease

TypeinterventionalSponsorShirley Ryan AbilityLabRan2017 to 2021Enrolled44ConditionsParkinson DiseaseArmsMotivational Interviewing, Web-based application
3 · Its place in the literature

Who cites it

95 citing papers in PubMed.

  1. NabioRxiv : the preprint server for biology · 2026
    Article
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  3. Review
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  13. Chrysin for Neurotrophic and Neurotransmitter Balance in Parkinson's Disease.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

35 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

4 authors.

Erwan BezardUniversity de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, Bordeaux, France. erwan.bezard@u-bordeaux2.fr
Zhenyu Yue
Deniz Kirik
Maria Grazia Spillantini

Funding

Using BAC-transgenic and Proteomic Approach to Study LRRK2 Biology and PathologyR01NS060809 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI YUE, ZHENYU · 2008 to 2017
$4.2M
Cellular and Molecular Basis for Initial PD Pathogenic Events in LRRK2 BAC ModelsR01NS072359 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BLITZER, ROBERT D., YUE, ZHENYU · 2011 to 2015
$1.8M
European Research Council 242932NINDS NIH HHS NS060809-01NINDS NIH HHS NS072359-01NINDS NIH HHS R01 NS060809NINDS NIH HHS R01 NS072359Parkinson's UK G-1102
6 · The paper itself

Abstract

Over the last two decades, significant strides has been made toward acquiring a better knowledge of both the etiology and pathogenesis of Parkinson's disease (PD). Experimental models are of paramount importance to obtain greater insights into the pathogenesis of the disease. Thus far, neurotoxin-based animal models have been the most popular tools employed to produce selective neuronal death in both in vitro and in vivo systems. These models have been commonly referred to as the pathogenic models. The current trend in modeling PD revolves around what can be called the disease gene-based models or etiologic models. The value of utilizing multiple models with a different mechanism of insult rests on the premise that dopamine-producing neurons die by stereotyped cascades that can be activated by a range of insults, from neurotoxins to downregulation and overexpression of disease-related genes. In this position article, we present the relevance of both pathogenic and etiologic models as well as the concept of clinically relevant designs that, we argue, should be utilized in the preclinical development phase of new neuroprotective therapies before embarking into clinical trials.

Indexed as

Disease Models, Animalalpha-SynucleinAnimalsGenetic VectorsHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2MiceMice, TransgenicMutationNeuroprotective AgentsNeurotoxinsParkinson DiseaseProtein Serine-Threonine Kinasesalpha-SynucleinLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanNeuroprotective AgentsNeurotoxinsProtein Serine-Threonine Kinases

Identifiers

PMID22753348
PMCPMC3517687

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.