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 mouse trisomy 16 brain.

L L Bambrick1, G Fiskum

  • 1Department of Anesthesiology, University of Maryland, School of Medicine, Baltimore, MD 21201, USA. lbambric@umaryland.edu

Brain Research
|December 7, 2007
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

Mechanisms of Musculoskeletal Frailty in People Living with HIV.

The Journal of frailty & aging·2022
Same author

Sex-dependent mitophagy and neuronal death following rat neonatal hypoxia-ischemia.

Neuroscience·2016
Same author

Anaesthetic neurotoxicity and neuroplasticity: an expert group report and statement based on the BJA Salzburg Seminar.

British journal of anaesthesia·2013
Same author

Mitochondrial detachment of hexokinase 1 in mood and psychotic disorders: implications for brain energy metabolism and neurotrophic signaling.

Journal of psychiatric research·2011
Same author

In vitro cell culture pO2 is significantly different from incubator pO2.

Biotechnology progress·2011
Same author

Methoxychlor causes mitochondrial dysfunction and oxidative damage in the mouse ovary.

Toxicology and applied pharmacology·2006
Same journal

IGFBP3 and UBE2C are associated with protein modification pathways and serve as prognostic markers in glioma.

Brain research·2026
Same journal

Targeting neurodevelopmental miR132-3p promotes neuroprotection and axon regeneration after optic nerve injury in mice.

Brain research·2026
Same journal

Variability in acoustic startle response and prepulse inhibition across adulthood in Fragile X messenger ribonucleoprotein 1 knockout mice.

Brain research·2026
Same journal

Transcriptome-guided modeling reveals insulin-related metabolic dysfunction in SCA3 mouse cerebellum.

Brain research·2026
Same journal

Intranasal stromal cell-derived factor-1α mitigates parkinsonian deficits via dual modulation of neuroinflammation and gut microbiota in MPTP-induced models.

Brain research·2026
Same journal

Emotions, the amygdala, and the right hemisphere.

Brain research·2026
See all related articles

Mitochondrial dysfunction in Down syndrome models shows reduced Complex I respiration and a key subunit decrease. This suggests shared mitochondrial pathology in neurodegenerative diseases like Parkinson's.

Area of Science:

  • Neuroscience
  • Mitochondrial Biology
  • Genetics

Background:

  • Down syndrome is associated with accelerated neuron death.
  • Mouse trisomy 16 (Ts16) serves as an animal model for Down syndrome.
  • Mitochondrial dysfunction is implicated in neurodegenerative processes.

Purpose of the Study:

  • To investigate mitochondrial function in the brain cortex of Ts16 mice.
  • To identify specific defects in the electron transport chain.
  • To explore potential links to other neurodegenerative conditions.

Main Methods:

  • Isolated cortex mitochondria were used for functional assays.
  • Oxygen consumption was measured using a Clarke electrode.
  • Western blotting was employed to quantify protein levels of electron transport chain subunits and pyruvate dehydrogenase.

Related Experiment Videos

Main Results:

  • A 16% decrease in respiration with Complex I substrates (malate, glutamate) was observed in Ts16 mitochondria.
  • A 20% reduction in the 20 kDa subunit of Complex I was detected.
  • Pyruvate dehydrogenase levels were decreased by 18% in Ts16 brain cortex.

Conclusions:

  • Ts16 mice exhibit specific Complex I deficits in brain mitochondria.
  • These mitochondrial alterations may contribute to accelerated neuron death in Down syndrome.
  • Shared mitochondrial pathology could be a common factor in neurodegenerative diseases, including Parkinson's disease.