Evidence map›Paper›PMID 28130586›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2018

Gene therapy approaches in the non-human primate model of Parkinson's disease.

D Pignataro, D Sucunza, A J Rico, I G Dopeso-Reyes, E Roda, A I Rodríguez-Perez, J L Labandeira-Garcia, V Broccoli, S Kato, K Kobayashi and 1 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Properties and Application of Pseudotyped Lentiviral Vectors.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Modeling Parkinson's Disease: Not Only Rodents?Frontiers in aging neuroscience · 2021
    Article
  11. Opportunities and limitations of genetically modified nonhuman primate models for neuroscience research.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Review
  12. Review
  13. Review
  14. Review
  15. Four main therapeutic keys for Parkinson's disease: A mini review.Iranian journal of basic medical sciences · 2019
    Review
  16. Review
  17. Angiotensin Type 1 Receptor Antagonists Protect Against Alpha-Synuclein-Induced Neuroinflammation and Dopaminergic Neuron Death.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018
    Article
  18. The use of nonhuman primate models to understand processes in Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2018
    Review
  19. Non-human primate research of basal ganglia and movement disorders: advances and challenges.Journal of neural transmission (Vienna, Austria : 1996) · 2018
    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

11 authors at 4 institutions in 3 countries.

D PignataroDepartment of Neurosciences, Center for Applied Medical Research (CIMA), University of Navarra, Pio XII Ave 55, Edificio CIMA, 31008, Pamplona, Navarra, Spain.
D SucunzaDepartment of Neurosciences, Center for Applied Medical Research (CIMA), University of Navarra, Pio XII Ave 55, Edificio CIMA, 31008, Pamplona, Navarra, Spain.
A J RicoDepartment of Neurosciences, Center for Applied Medical Research (CIMA), University of Navarra, Pio XII Ave 55, Edificio CIMA, 31008, Pamplona, Navarra, Spain.
I G Dopeso-ReyesDepartment of Neurosciences, Center for Applied Medical Research (CIMA), University of Navarra, Pio XII Ave 55, Edificio CIMA, 31008, Pamplona, Navarra, Spain.
E RodaDepartment of Neurosciences, Center for Applied Medical Research (CIMA), University of Navarra, Pio XII Ave 55, Edificio CIMA, 31008, Pamplona, Navarra, Spain.
A I Rodríguez-PerezCentro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain.
J L Labandeira-GarciaCentro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain.
V BroccoliDivision of Neuroscience, Ospedale San Raffaele, 20132, Milan, Italy.
S KatoDepartment of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, Fukushima, Japan.
K KobayashiDepartment of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, Fukushima, Japan.
José L LanciegoDepartment of Neurosciences, Center for Applied Medical Research (CIMA), University of Navarra, Pio XII Ave 55, Edificio CIMA, 31008, Pamplona, Navarra, Spain. jlanciego@unav.es.ORCID 0000-0003-2301-5419
Biomedical Research Networking Center on Neurodegenerative Diseases · ESFukushima Medical University · JPUniversidade de Santiago de Compostela · ESNeuroscience Institute · IT

Funding

CiberNed 2014/01European Research Council 340527Fundació la Marató de TV3 (ES) 20141331Spanish Ministry of Economy and Competitiveness BFU2012-27907
6 · The paper itself

Abstract

The field of gene therapy has recently witnessed a number of major conceptual changes. Besides the traditional thinking that comprises the use of viral vectors for the delivery of a given therapeutic gene, a number of original approaches have been recently envisaged, focused on using vectors carrying genes to further modify basal ganglia circuits of interest. It is expected that these approaches will ultimately induce a therapeutic potential being sustained by gene-induced changes in brain circuits. Among others, at present, it is technically feasible to use viral vectors to (1) achieve a controlled release of neurotrophic factors, (2) conduct either a transient or permanent silencing of any given basal ganglia circuit of interest, (3) perform an in vivo cellular reprogramming by promoting the conversion of resident cells into dopaminergic-like neurons, and (4) improving levodopa efficacy over time by targeting aromatic L-amino acid decarboxylase. Furthermore, extensive research efforts based on viral vectors are currently ongoing in an attempt to better replicate the dopaminergic neurodegeneration phenomena inherent to the progressive intraneuronal aggregation of alpha-synuclein. Finally, a number of incoming strategies will soon emerge over the horizon, these being sustained by the underlying goal of promoting alpha-synuclein clearance, such as, for instance, gene therapy initiatives based on increasing the activity of glucocerebrosidase. To provide adequate proof-of-concept on safety and efficacy and to push forward true translational initiatives based on these different types of gene therapies before entering into clinical trials, the use of non-human primate models undoubtedly plays an instrumental role.

Indexed as

Genetic TherapyGenetic Vectorsalpha-SynucleinAnimalsDisease Models, AnimalParkinson DiseasePrimatesalpha-SynucleinBasal gangliaDopamineDyskinesiaMacaquesNeurodegenerationViral vectors

Identifiers

PMID28130586
OpenAlexW2582829583

What OpenQuestion holds

Textmetadata
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.