• HOME
  • NEWS
  • EXPLORE
    • CAREER
      • Companies
      • Jobs
    • EVENTS
    • iGEM
      • News
      • Team
    • PHOTOS
    • VIDEO
    • WIKI
  • BLOG
  • COMMUNITY
    • FACEBOOK
    • INSTAGRAM
    • TWITTER
Monday, July 21, 2025
BIOENGINEER.ORG
No Result
View All Result
  • Login
  • HOME
  • NEWS
  • EXPLORE
    • CAREER
      • Companies
      • Jobs
        • Lecturer
        • PhD Studentship
        • Postdoc
        • Research Assistant
    • EVENTS
    • iGEM
      • News
      • Team
    • PHOTOS
    • VIDEO
    • WIKI
  • BLOG
  • COMMUNITY
    • FACEBOOK
    • INSTAGRAM
    • TWITTER
  • HOME
  • NEWS
  • EXPLORE
    • CAREER
      • Companies
      • Jobs
        • Lecturer
        • PhD Studentship
        • Postdoc
        • Research Assistant
    • EVENTS
    • iGEM
      • News
      • Team
    • PHOTOS
    • VIDEO
    • WIKI
  • BLOG
  • COMMUNITY
    • FACEBOOK
    • INSTAGRAM
    • TWITTER
No Result
View All Result
Bioengineer.org
No Result
View All Result
Home NEWS Science News Health

New study gives clue to the cause, and possible treatment of Parkinson’s Disease

Bioengineer by Bioengineer
June 10, 2021
in Health
Reading Time: 3 mins read
0
ADVERTISEMENT
Share on FacebookShare on TwitterShare on LinkedinShare on RedditShare on Telegram

Zebrafish model research reveals clues about molecular triggers of Parkinson’s Disease

IMAGE

Credit: Matsui et al., Nat Commun. 2021

Niigata, Japan – Researchers from Brain Research Institute, Niigata University, Japan may have unraveled a new approach that could revolutionize the treatment, prevention, and possibly reversal of the damages that could lead to Parkinson’s Disease (PD). This novel finding utilizing the cellular and zebrafish models, demonstrated how the leakage of mitochondrial dsDNA into the cytosol environment of the cell can contribute to the impairment of brain tissue of patients with PD.

Parkinson’s disease is the second most common neurodegenerative disease, and its prevalence has been projected to double over the next 30 years.

These sobering statistics and the quest for PD prognostic marker discovery inspired a team of scientists led by Prof. Hideaki Matsui to build upon previous knowledge that link mitochondrial dysfunction and lysosomal dysfunction to PD. In an interview Prof. Matsui said, “Our results showed for the first time that cytosolic dsDNA of mitochondrial origin leaking and escaping from lysosomal degradation can induce cytotoxicity both in cultured cells, as well as in zebrafish models of Parkinson’s disease.”

Prof. Matsui went on to explain that “This study showed that the leakage of this mitochondrial nucleic material may occur as a result of mitochondrial dysfunction, which may involve genetic mutations in genes encoding mitochondrial proteins or incomplete degradation of mitochondrial dsDNA in the lysosome – which is a “degradation factory” of the cell. Upon the leakage into the cytoplasm, this undegraded dsDNA is detected by a “foreign” DNA sensor of the cytoplasm (IFI16) which then triggers the upregulation of mRNAs encoding for inflammatory proteins (type I interferon stimulated cytokines such as IL1β). Although further investigation is required, we hypothesize that the subsequent accumulation of inflammatory protein within the cytoplasm, may cause cell functional imbalance and ultimately cell death.”

“However, this dsDNA leakage effect can be counteracted by DNAse II, a dsDNA degrading agent.”, Prof. Akiyoshi Kakita, who was an associate investigator in the study also added.

The first part of the study was conducted in vitro, using cells of nerve cancer origin (SH-SY5Y cells) with defective mitochondria and lysosomal dysfunctions through knockdown of GBA, ATP13A and PINK1 genes. The mutant cells demonstrated leakage of dsDNA and accumulation of inflammatory cytokines and cell death. In an additional comparison experiment using mutant cells (with defective mitochondrial proteins) and wild type SH-SY5Y cells, they further demonstrated that DNAse II rescued cells through the degradation of dsDNA.

In a confirmatory study using a PD zebrafish model (gba mutant), the researchers demonstrated that a combination of PD-like phenotypes including accumulation of cytosol dsDNA deposits, reduced number of dopaminergic neurons after 3 months. Lastly, they further generated a DNase II mutant zebrafish model which exhibited decreased numbers of dopaminergic neurons and demonstrated accumulated cytosolic DNA. Interestingly, when then gba mutant zebrafish was complemented with human DNAse II gene, the overexpression of human DNAse II decreased cytosolic dsDNA deposits, rescued neuro-degradation by rescuing the number of dopaminergic and noradrenergic neurons after 3 months.

This demonstrated that neurodegenerative phenotype of gba mutant zebrafish induced by dsDNA deposits in the cytosol can be restored by DNAse II.

In a step further, to determine the effect of cytosolic dsDNA of mitochondrial origin in human brain with PD, they inspected postmortem human brain tissues from patients who were diagnosed with idiopathic PD. They observed abundance of cytosolic dsDNA of mitochondrial origin in medulla oblongata of postmortem brain tissues, the levels of IFI16 were also markedly increased in these brain tissues. Taken together, results in this study demonstrated that cytosolic dsDNA of mitochondrial origin accumulated in PD brains and that these dsDNA deposits and IFI16 play contributory roles in human PD pathogenesis.

###

The article “Cytosolic dsDNA of mitochondrial origin induces cytotoxicity and neurodegeneration in cellular and zebrafish models of Parkinson’s disease” was published in NATURE COMMUNICATIONS at https://doi.org/10.1038/s41467-021-23452-x.

Media Contact
Hideaki Matsui

hide0729@bri.niigata-u.ac.jp

Original Source

https://www.bri.niigata-u.ac.jp/en/research/result/001547.html

Related Journal Article

http://dx.doi.org/10.1038/s41467-021-23452-x

Tags: BiologyCell BiologyGeneticsMedicine/HealthMolecular BiologyneurobiologyParkinson
Share12Tweet8Share2ShareShareShare2

Related Posts

Single-Cell Atlas Links Chemokines to Type 2 Diabetes

July 20, 2025
blank

AI Diagnoses Structural Heart Disease via ECG

July 17, 2025

Functional Regimes Shape Soil Microbiome Response

July 17, 2025

Stealth Adaptations in Large Ichthyosaur Flippers

July 17, 2025
Please login to join discussion

POPULAR NEWS

  • Enhancing Broiler Growth: Mannanase Boosts Performance with Reduced Soy and Energy

    Enhancing Broiler Growth: Mannanase Boosts Performance with Reduced Soy and Energy

    73 shares
    Share 29 Tweet 18
  • New Organic Photoredox Catalysis System Boosts Efficiency, Drawing Inspiration from Photosynthesis

    54 shares
    Share 22 Tweet 14
  • IIT Researchers Unveil Flying Humanoid Robot: A Breakthrough in Robotics

    53 shares
    Share 21 Tweet 13
  • Overlooked Dangers: Debunking Common Myths About Skin Cancer Risk in the U.S.

    52 shares
    Share 21 Tweet 13

About

BIOENGINEER.ORG

We bring you the latest biotechnology news from best research centers and universities around the world. Check our website.

Follow us

Recent News

Additive Manufacturing of Monolithic Gyroidal Solid Oxide Cells

Machine Learning Uncovers Sorghum’s Complex Mold Resistance

Pathology Multiplexing Revolutionizes Disease Mapping

  • Contact Us

Bioengineer.org © Copyright 2023 All Rights Reserved.

Welcome Back!

Login to your account below

Forgotten Password?

Retrieve your password

Please enter your username or email address to reset your password.

Log In
No Result
View All Result
  • Homepages
    • Home Page 1
    • Home Page 2
  • News
  • National
  • Business
  • Health
  • Lifestyle
  • Science

Bioengineer.org © Copyright 2023 All Rights Reserved.