Evidence map›Paper›PMID 25565980›Full record

ReviewFrontiers in neuroanatomy2014

Parkinson's disease: animal models and dopaminergic cell vulnerability.

Javier Blesa, Serge Przedborski

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroanatomy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 243 papers.

0numbers the graph read from it
0cells of the map it votes in
243citing papers in PubMed
22.5field-weighted citation impact, top 1% 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

243 citing papers in PubMed, 462 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Neuroprotective Potential of Synaptamide in MPTP-Induced Parkinson's Disease.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Article
  5. Article
  6. Modulation of hierarchical motor sequence learning by alpha-synuclein and the adenosine ANeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  7. Article
  8. Article
  9. Article
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  12. Targeting ASK1 signaling in neurodegeneration: molecular insights and therapeutic promise.Apoptosis : an international journal on programmed cell death · 2025
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Mitochondrial Dysfunction in Genetic and Non-Genetic Parkinson's Disease.International journal of molecular sciences · 2025
    Review
  20. Review

183 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

2 authors at 1 institution in 1 country.

Javier BlesaDepartment of Pathology and Cell Biology, Center for Motor Neuron Biology and Disease, College of Physicians and Surgeons, Columbia University New York, NY, USA.
Serge PrzedborskiDepartment of Pathology and Cell Biology, Center for Motor Neuron Biology and Disease, College of Physicians and Surgeons, Columbia University New York, NY, USA.
Columbia University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder that affects about 1.5% of the global population over 65 years of age. A hallmark feature of PD is the degeneration of the dopamine (DA) neurons in the substantia nigra pars compacta (SNc) and the consequent striatal DA deficiency. Yet, the pathogenesis of PD remains unclear. Despite tremendous growth in recent years in our knowledge of the molecular basis of PD and the molecular pathways of cell death, important questions remain, such as: (1) why are SNc cells especially vulnerable; (2) which mechanisms underlie progressive SNc cell loss; and (3) what do Lewy bodies or α-synuclein reveal about disease progression. Understanding the variable vulnerability of the dopaminergic neurons from the midbrain and the mechanisms whereby pathology becomes widespread are some of the primary objectives of research in PD. Animal models are the best tools to study the pathogenesis of PD. The identification of PD-related genes has led to the development of genetic PD models as an alternative to the classical toxin-based ones, but does the dopaminergic neuronal loss in actual animal models adequately recapitulate that of the human disease? The selection of a particular animal model is very important for the specific goals of the different experiments. In this review, we provide a summary of our current knowledge about the different in vivo models of PD that are used in relation to the vulnerability of the dopaminergic neurons in the midbrain in the pathogenesis of PD.

Indexed as

6-OHDAATP13A2DJ1LRRK2MPTPparkinrotenonesynuclein

Identifiers

PMID25565980
PMCPMC4266040
OpenAlexW2097830904

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.