Evidence map›Paper›PMID 32470327›Full record

ArticleStem cell reports2020

Identifying Therapeutic Agents for Amelioration of Mitochondrial Clearance Disorder in Neurons of Familial Parkinson Disease.

Akihiro Yamaguchi, Kei-Ichi Ishikawa, Tsuyoshi Inoshita, Kahori Shiba-Fukushima, Shinji Saiki, Taku Hatano, Akio Mori, Yutaka Oji, Ayami Okuzumi, Yuanzhe Li and 4 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Stem Cell-Based Approaches in Parkinson's Disease Research.International journal of stem cells · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. PINK1 and Parkin regulate IPNature communications · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Reduced ER-mitochondrial contact sites and mitochondrial CaFrontiers in cell and developmental biology · 2023
    Article
  18. Review
  19. Article
  20. 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

14 authors at 1 institution in 1 country.

Akihiro YamaguchiCenter for Genomic and Regenerative Medicine, Juntendo University Graduate School of Medicine, Tokyo 113-8431, Japan.
Kei-Ichi IshikawaCenter for Genomic and Regenerative Medicine, Juntendo University Graduate School of Medicine, Tokyo 113-8431, Japan; Department of Neurology, Juntendo University School of Medicine, Tokyo 113-8431, Japan. Electronic address: kishikaw@juntendo.ac.jp.
Tsuyoshi InoshitaDepartment of Treatment and Research in Multiple Sclerosis and Neuro-intractable Disease, Tokyo 113-8431, Japan.
Kahori Shiba-FukushimaDepartment of Treatment and Research in Multiple Sclerosis and Neuro-intractable Disease, Tokyo 113-8431, Japan.
Shinji SaikiDepartment of Neurology, Juntendo University School of Medicine, Tokyo 113-8431, Japan.
Taku HatanoDepartment of Neurology, Juntendo University School of Medicine, Tokyo 113-8431, Japan.
Akio MoriDepartment of Neurology, Juntendo University School of Medicine, Tokyo 113-8431, Japan.
Yutaka OjiDepartment of Neurology, Juntendo University School of Medicine, Tokyo 113-8431, Japan.
Ayami OkuzumiDepartment of Neurology, Juntendo University School of Medicine, Tokyo 113-8431, Japan.
Yuanzhe LiDepartment of Neurology, Juntendo University School of Medicine, Tokyo 113-8431, Japan.
Manabu FunayamaCenter for Genomic and Regenerative Medicine, Juntendo University Graduate School of Medicine, Tokyo 113-8431, Japan; Department of Neurology, Juntendo University School of Medicine, Tokyo 113-8431, Japan; Research Institute for Diseases of Old Age, Graduate School of Medicine, Juntendo University, Tokyo 113-8421, Japan.
Yuzuru ImaiDepartment of Neurology, Juntendo University School of Medicine, Tokyo 113-8431, Japan; Department of Research for Parkinson's Disease, Juntendo University Graduate School of Medicine, Tokyo 113-8431, Japan.
Nobutaka HattoriDepartment of Neurology, Juntendo University School of Medicine, Tokyo 113-8431, Japan; Department of Treatment and Research in Multiple Sclerosis and Neuro-intractable Disease, Tokyo 113-8431, Japan; Department of Research for Parkinson's Disease, Juntendo University Graduate School of Medicine, Tokyo 113-8431, Japan.
Wado AkamatsuCenter for Genomic and Regenerative Medicine, Juntendo University Graduate School of Medicine, Tokyo 113-8431, Japan. Electronic address: awado@juntendo.ac.jp.
Juntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson disease (PD) is a neurodegenerative disorder caused by the progressive loss of midbrain dopaminergic neurons, and mitochondrial dysfunction is involved in its pathogenesis. This study aimed to establish an imaging-based, semi-automatic, high-throughput system for the quantitative detection of disease-specific phenotypes in dopaminergic neurons from induced pluripotent stem cells (iPSCs) derived from patients with familial PD having Parkin or PINK1 mutations, which exhibit abnormal mitochondrial homeostasis. The proposed system recapitulates the deficiency of mitochondrial clearance, ROS accumulation, and increasing apoptosis in these familial PD-derived neurons. We screened 320 compounds for their ability to ameliorate multiple phenotypes and identified four candidate drugs. Some of these drugs improved the locomotion defects and reduced ATP production caused by PINK1 inactivation in Drosophila and were effective for idiopathic PD-derived neurons with impaired mitochondrial clearance. Our findings suggest that the proposed high-throughput system has potential for identifying effective drugs for familial and idiopathic PD.

Indexed as

AnimalsApoptosisCell LineCells, CulturedDopaminergic NeuronsDrosophila melanogasterDrug DiscoveryHigh-Throughput Screening AssaysHumansInduced Pluripotent Stem CellsMitochondriaMutationNeurogenesisNeuroprotective AgentsParkinson DiseasePhenotypeNeuroprotective Agentsparkin proteinProtein KinasesPTEN-Induced Putative KinaseReactive Oxygen SpeciesUbiquitin-Protein Ligasesdrug screeningiPS cellsmitochondriamitophagyPARK2PARK6Parkinson disease

Identifiers

PMID32470327
PMCPMC7355139
OpenAlexW3031142363

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.