Evidence map›Paper›PMID 27638713›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2017

Gene therapy targeting mitochondrial pathway in Parkinson's disease.

Chi-Jing Choong, Hideki Mochizuki

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review
  3. Review
  4. Targeting Mitochondrial Complex I Deficiency in MPPBiological procedures online · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. MiR-193b deregulation is associated with Parkinson's disease.Journal of cellular and molecular medicine · 2021
    Article
  10. Genotype-driven therapeutic developments in Parkinson's disease.Molecular medicine (Cambridge, Mass.) · 2021
    Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Novel Approaches for the Treatment of Alzheimer's and Parkinson's Disease.International journal of molecular sciences · 2019
    Review
  17. Article
  18. Salidroside Protects against MPP+-Induced Neuronal Injury through DJ-1-Nrf2 Antioxidant Pathway.Evidence-based complementary and alternative medicine : eCAM · 2017
    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

2 authors at 1 institution in 1 country.

Chi-Jing ChoongDepartment of Neurology, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita, Osaka, 565-0871, Japan.
Hideki MochizukiDepartment of Neurology, Graduate School of Medicine, Osaka University, Yamadaoka 2-2, Suita, Osaka, 565-0871, Japan. hmochizuki@neurol.med.osaka-u.ac.jp.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) presents a relative selective localization of pathology to substantia nigra and well-defined motor symptoms caused by dopaminergic degeneration that makes it an ideal target for gene therapy. Parallel progress in viral vector systems enables the delivery of therapeutic genes directly into brain with reasonable safety along with sustained transgene expression. To date, gene therapy for PD that has reached clinical trial evaluation is mainly based on symptomatic approach that involves enzyme replacement strategy and restorative approach that depends on the addition of neurotrophic factors. Mitochondrial dysregulation, such as reduced complex I activity, increased mitochondria-derived reactive oxygen species (ROS) production, ROS-mediated mitochondrial DNA damage, bioenergetic failure, and perturbation of mitochondrial dynamics and mitophagy, has long been implicated in the pathogenesis of PD. Many of mutated genes linked to familial forms of PD affect these mitochondrial features. In this review, we discuss the recent progress that has been made in preclinical development of gene therapy targeting the mitochondrial pathway as disease modifying approach for PD. This review focuses on the potential therapeutic efficacy of candidate genes, including Parkin, PINK1, alpha synuclein, PGC-1 alpha, and anti-apoptotic molecules.

Indexed as

Genetic TherapyAnimalsApoptosisHumansMitochondriaParkinson DiseaseAlpha synucleinGene therapyMitochondrial dysfunctionParkinParkinson’s diseasePGC-1 alphaPINK1

Identifiers

PMID27638713
OpenAlexW2520626539

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.