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 movement disorders

J B Schulz1, M F Beal

  • 1Harvard Medical School, Boston, Massachusetts.

Current Opinion in Neurology
|August 1, 1994
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

An Unusual Presentation of Peri-Lead Edema Following Deep Brain Stimulation for Parkinson's Disease: A Case Report and Review of the Literature.

Clinical case reports·2025
Same author

Modulating the cholinergic system-Novel targets for deep brain stimulation in Parkinson's disease.

Journal of neurochemistry·2024
Same author

Gait improvement by high-frequency stimulation of the subthalamic nucleus in Parkinsonian mice is not associated with changes of the cholinergic system in the pedunculopontine nucleus.

Neuroscience letters·2023
Same author

Causes of Death in Endovascularly Treated Patients with Acute Stroke.

AJNR. American journal of neuroradiology·2022
Same author

[ZSE-DUO - dual guidance structure at the centre for rare diseases].

Innere Medizin (Heidelberg, Germany)·2022
Same author

Endovascular stroke treatment does not preclude high thrombolysis rates.

European journal of neurology·2018
Same journal

Multimodal mapping of balance dysfunction in Parkinson's disease: a consensus roadmap for research and intervention.

Current opinion in neurology·2026
Same journal

Tourette syndrome: brain neurophysiology, circuit dysfunction, and neuromodulation across invasive and noninvasive approaches.

Current opinion in neurology·2026
Same journal

Dystonia: from phenotypes to genetics and therapeutic advances.

Current opinion in neurology·2026
Same journal

What can we learn from eye movements in movement disorders and Parkinson's disease?

Current opinion in neurology·2026
Same journal

Functional movement disorders: diagnosis, pathophysiology, and treatment.

Current opinion in neurology·2026
Same journal

Galectins in the brain: advances in neuroinflammation, neuroprotection and therapeutic opportunities: Erratum.

Current opinion in neurology·2026
See all related articles

Mitochondrial defects are implicated in movement disorders like Parkinson's and Huntington's disease. Studies show mitochondrial dysfunction contributes to neuronal degeneration, suggesting a direct role in disease pathogenesis.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Genetics

Background:

  • Mitochondrial dysfunction is a leading theory in neurodegenerative movement disorders.
  • Defects in oxidative phosphorylation enzymes are observed in Parkinson's, Huntington's, and other conditions.
  • Mitochondrial DNA deletions accumulate with age, particularly in susceptible brain regions.

Purpose of the Study:

  • To investigate the role of mitochondrial defects in movement disorder pathogenesis.
  • To explore biochemical and animal models of neurodegeneration.

Main Methods:

  • Biochemical analysis of postmortem tissues, platelets, muscle, and lymphocytes.
  • Utilizing animal models, including the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model for Parkinson's disease.

Related Experiment Videos

  • Employing the complex II inhibitor 3-nitropropionic acid (3-NP) to model Huntington's disease.

    • Main Results:

    • Biochemical studies reveal defects in oxidative phosphorylation enzymes across various movement disorders.
    • MPTP model demonstrates inhibition of Complex I of the electron transport chain.
    • 3-NP administration successfully replicates key features of Huntington's disease in animal models, suggesting excitotoxicity as a mechanism.

    Conclusions:

    • Both direct biochemical evidence and animal models strongly support mitochondrial dysfunction as a key factor in movement disorder development.
    • Targeting mitochondrial pathways may offer therapeutic strategies for neurodegenerative movement disorders.