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

beta-Amyloid-induced cerebrovascular endothelial dysfunction

T Thomas1, C McLendon, E T Sutton

  • 1Department of Psychiatry, College of Medicine, University of South Florida, Tampa 33613, USA.

Annals of the New York Academy of Sciences
|November 5, 1997
PubMed
Summary

Beta-amyloid causes cerebrovascular damage by harming artery lining and reducing blood flow, potentially contributing to Alzheimer's disease. This damage is linked to reactive oxygen radicals.

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

Physiological levels of beta-amyloid induce cerebral vessel dysfunction and reduce endothelial nitric oxide production.

Neurological research·2001
Same author

Cell-free assays for gamma-secretase activity.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology·2000
Same author

Potassium channel openers prevent beta-amyloid toxicity in bovine vascular endothelial cells.

Neuroscience letters·2000
Same author

Animal model of Alzheimer-like vascular pathology and inflammatory reaction.

Annals of the New York Academy of Sciences·2000
Same author

Estrogen protects peripheral and cerebral blood vessels from toxicity of Alzheimer peptide amyloid-beta and inflammatory reaction.

Journal of submicroscopic cytology and pathology·2000
Same author

Pulmonary endothelial and epithelial integrity and neutrophil infiltration after endotoxin in interleukin-1 receptor knockout mice.

Shock (Augusta, Ga.)·2000

Area of Science:

  • Neuroscience
  • Vascular Biology
  • Biochemistry

Background:

  • Alzheimer's disease is a neurodegenerative disorder.
  • Cerebrovascular dysfunction is implicated in Alzheimer's pathogenesis.
  • Beta-amyloid is a key protein aggregate in Alzheimer's disease.

Purpose of the Study:

  • To investigate the cerebrovascular effects of beta-amyloid.
  • To determine the mechanisms of beta-amyloid-induced vascular damage.
  • To explore the role of beta-amyloid in early Alzheimer's pathology.

Main Methods:

  • Experiments conducted on bovine mid-cerebral arteries.
  • Assessment of vasoconstriction and vasodilation responses.
  • Electron microscopy to visualize endothelial damage.

Related Experiment Videos

  • Investigation of reactive oxygen radical involvement.

    • Main Results:

    • Beta-amyloid induced significant endothelial damage in cerebral arteries.
    • Observed were increased vasoconstriction and diminished vasodilation.
    • Electron microscopy confirmed structural endothelial alterations.
    • Reactive oxygen radicals were identified as mediators of the dysfunction.

    Conclusions:

    • Beta-amyloid directly damages cerebrovascular endothelium.
    • This vascular damage, mediated by oxidative stress, may be an early pathological event in Alzheimer's disease.
    • Findings highlight the link between beta-amyloid, vascular health, and Alzheimer's development.