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 amyloid-beta peptide: pathogenesis or late-phase development?

Shi Du Yan1, Wen-Cheng Xiong, David M Stern

  • 1Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.

Journal of Alzheimer'S Disease : JAD
|July 29, 2006
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

Astrocytic VPS35 coordinates iron homeostasis with HIF1α-VEGFa signaling to prevent astrocytic ferroptosis and to promote neocortical angiogenesis.

Cell & bioscience·2026
Same author

A Skull Bone Marrow-to-Brain Axis Links Osteoblastic Activity to Myeloid Cell Trafficking, Cerebral Blood Flow, and Cognition in Alzheimer's Progression.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

Role of extracellular vesicles derived from HIV-infected T cells and microglial cells in neuroinflammation and neuropathogenesis using a blood-brain barrier and cerebral organoid co-culture model.

Journal of neurovirology·2026
Same author

Cortical astrocytic neogenin, a key protein switching HIF1/2ɑ-VEGFa-induced angiogenesis to MEGF10-driven phagocytosis.

Cell reports·2026
Same author

LRP4+ Astrocytes: A Unique Subpopulation Crucial for Blood Vessel Maintenance and Function in the Somatosensory Cortex of Normal and 5xFAD Mice.

Glia·2025
Same author

Neuronal MCT2 promotes angiogenesis via lactate in the developing mouse neocortex.

Cell death and differentiation·2025

Mitochondrial dysfunction is implicated in Alzheimer's disease (AD), potentially driven by amyloid-beta within mitochondria. This dysfunction likely contributes to the oxidative stress observed in AD brains.

Area of Science:

  • Neuroscience
  • Mitochondrial Biology
  • Neurodegenerative Diseases

Background:

  • Mitochondrial and metabolic dysfunction are increasingly linked to Alzheimer's disease (AD).
  • Key questions remain about whether these metabolic changes are a cause or consequence of neuronal degeneration in AD.
  • Altered mitochondrial function in AD may stem from intrinsic factors (e.g., mitochondrial DNA mutations) or extrinsic signaling pathways.

Purpose of the Study:

  • To review current data on the role of mitochondria in Alzheimer's disease.
  • To explore the mechanisms underlying mitochondrial dysfunction in AD.
  • To consider the implications of amyloid-beta's presence within mitochondria.

Main Methods:

  • Literature review of studies investigating mitochondrial function in Alzheimer's disease.

Related Experiment Videos

  • Analysis of findings related to amyloid-beta interactions within mitochondria.
  • Examination of the link between mitochondrial dysfunction and oxidative stress in AD models.

    • Main Results:

    • Amyloid-beta peptide has been found within mitochondria in AD.
    • Amyloid-beta interacts with molecular targets inside mitochondria.
    • Mitochondrial dysfunction is a likely contributor to the oxidative stress characteristic of AD.

    Conclusions:

    • Mitochondrial dysfunction is a significant factor in Alzheimer's disease pathogenesis.
    • Amyloid-beta's presence and interaction within mitochondria are critical areas of investigation.
    • Mitochondrial dysfunction contributes to the oxidative stress observed in Alzheimer's disease.