Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Mitochondrial dysfunction in neurodegeneration

J M Cooper1, A H Schapira

  • 1Clinical Neurosciences, Royal Free Hospital School of Medicine, London, United Kingdom.

Journal of Bioenergetics and Biomembranes
|April 1, 1997
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Creating tissue on chip constructs in microtitre plates for drug discovery.

RSC advances·2022
Same author

Effects of ambroxol on the autophagy-lysosome pathway and mitochondria in primary cortical neurons.

Scientific reports·2018
Same author

Desvenlafaxine overdose and the occurrence of serotonin toxicity, seizures and cardiovascular effects.

Clinical toxicology (Philadelphia, Pa.)·2016
Same author

Corrigendum: Visualization of Surface Acoustic Waves in Thin Liquid Films.

Scientific reports·2016
Same author

Visualization of Surface Acoustic Waves in Thin Liquid Films.

Scientific reports·2016
Same author

Assessment of biocompatibility of 3D printed photopolymers using zebrafish embryo toxicity assays.

Lab on a chip·2015
Same journal

Sinomenine protects against oxidized low-density lipoprotein-induced human umbilical vein endothelial cell injury through regulating the myocyte enhancer factor 2 A/C-X-C motif chemokine ligand 14 pathway.

Journal of bioenergetics and biomembranes·2026
Same journal

DNMT1 methylates E3 ligase FBXO32 to regulate Myc stability and glycolytic reprogramming in diabetic retinopathy associated endothelial cells.

Journal of bioenergetics and biomembranes·2026
Same journal

Targeting MEK1/2 inhibits mitochondrial respiration and redox homeostasis in resistant rectal cancer.

Journal of bioenergetics and biomembranes·2026
Same journal

Intestinal microecology regulates neutrophil recruitment through TLR4/MAPK/CXCR2 signaling pathway to promote liver ischemia/reperfusion injury.

Journal of bioenergetics and biomembranes·2026
Same journal

Integrating weighted gene co-expression network analysis and machine learning reveal that NDUFA4L2 alleviates KA-induced HT22 cell neurotoxicity, apoptosis, oxidative stress, and mitochondrial dysfunction.

Journal of bioenergetics and biomembranes·2026
Same journal

The FOXO3/ZC3H13/SLC3A2 cascade modulates the osteogenic differentiation and ferroptosis of BMSCs.

Journal of bioenergetics and biomembranes·2026
See all related articles

Mitochondrial toxins can cause neurodegenerative diseases like Parkinson's and Huntington's. Understanding these toxins offers potential for developing new neuroprotective treatments.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Toxicology

Background:

  • Mitochondrial respiratory chain dysfunction is implicated in numerous toxins.
  • Toxins interfering with mitochondrial function are used in pesticides and herbicides.
  • Accidental human exposure to toxins has yielded valuable animal models for human diseases.

Purpose of the Study:

  • To explore the role of mitochondrial toxins in neuronal cell death.
  • To investigate the biochemical similarities between toxin-induced models and idiopathic neurodegenerative diseases.
  • To assess the potential for therapeutic interventions targeting mitochondrial dysfunction.

Main Methods:

  • Review of existing literature on mitochondrial toxins and neurodegenerative diseases.
  • Analysis of primate models induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 3-nitropropionic acid (3-NPA).

Related Experiment Videos

  • Comparison of biochemical deficiencies in animal models with those in human patients.

    • Main Results:

    • MPTP and 3-NPA exposure in primates created models for Parkinson's and Huntington's diseases, respectively.
    • Identical biochemical deficiencies were observed in affected human brain regions and toxin-induced models.
    • Complex I deficiency is potentially a primary factor in some Parkinson's disease cases.
    • Complex II/III deficiency in Huntington's disease appears secondary.

    Conclusions:

    • Mitochondrial toxins provide critical insights into neurodegenerative disease mechanisms.
    • Therapeutic strategies targeting mitochondrial dysfunction hold promise for neuroprotection.
    • Further research is needed to clarify the role of specific mitochondrial complex deficiencies in idiopathic diseases.