Evidence map›Paper›PMID 25759364›Full record

ArticleEMBO molecular medicine2015

Combined Nurr1 and Foxa2 roles in the therapy of Parkinson's disease.

Sang-Min Oh, Mi-Yoon Chang, Jae-Jin Song, Yong-Hee Rhee, Eun-Hye Joe, Hyun-Seob Lee, Sang-Hoon Yi, Sang-Hun Lee

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 92 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Sang-Min OhDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea Hanyang Biomedical Research Institute, Hanyang University, Seoul, Korea Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Korea.
Mi-Yoon ChangHanyang Biomedical Research Institute, Hanyang University, Seoul, Korea.
Jae-Jin SongDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea Hanyang Biomedical Research Institute, Hanyang University, Seoul, Korea Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Korea.
Yong-Hee RheeDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea Hanyang Biomedical Research Institute, Hanyang University, Seoul, Korea Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Korea.
Eun-Hye JoeDepartment of Phamacology, Ajou University School of Medicine, Suwon, Korea.
Hyun-Seob LeeDepartment of Applied Bioscience, College of Life Science, CHA University, Seoul, Korea.
Sang-Hoon YiHanyang Biomedical Research Institute, Hanyang University, Seoul, Korea sanghooni@hanmail.net leesh@hanyang.ac.kr.
Sang-Hun LeeDepartment of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, Seoul, Korea Hanyang Biomedical Research Institute, Hanyang University, Seoul, Korea Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Korea sanghooni@hanmail.net leesh@hanyang.ac.kr.
Hanyang University Medical Center · KRHanyang University · KRAjou University · KRCHA University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Use of the physiological mechanisms promoting midbrain DA (mDA) neuron survival seems an appropriate option for developing treatments for Parkinson's disease (PD). mDA neurons are specifically marked by expression of the transcription factors Nurr1 and Foxa2. We show herein that Nurr1 and Foxa2 interact to protect mDA neurons against various toxic insults, but their expression is lost during aging and degenerative processes. In addition to their proposed cell-autonomous actions in mDA neurons, forced expression of these factors in neighboring glia synergistically protects degenerating mDA neurons in a paracrine mode. As a consequence of these bimodal actions, adeno-associated virus (AAV)-mediated gene delivery of Nurr1 and Foxa2 in a PD mouse model markedly protected mDA neurons and motor behaviors associated with nigrostriatal DA neurotransmission. The effects of the combined gene delivery were dramatic, highly reproducible, and sustained for at least 1 year, suggesting that expression of these factors is a promising approach in PD therapy.

Indexed as

AnimalsCells, CulturedDisease Models, AnimalDopaminergic NeuronsGenetic TherapyHepatocyte Nuclear Factor 3-betaMaleMesencephalonMice, Inbred ICRNeurogliaNuclear Receptor Subfamily 4, Group A, Member 2Parkinson DiseaseTreatment OutcomeFoxa2 protein, mouseHepatocyte Nuclear Factor 3-betaNr4a2 protein, mouseNuclear Receptor Subfamily 4, Group A, Member 2Foxa2gene therapymidbrain dopamine neuronNurr1Parkinson's disease

Identifiers

PMID25759364
PMCPMC4492814
OpenAlexW2103575789

What OpenQuestion holds

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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.