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

Interrelationship between beta-amyloid deposition and complement-activated oligodendroglia

T Yamada1, Y Tsuboi, M Takahashi

  • 1Department of Neurology, Chiba University, Japan.

Dementia and Geriatric Cognitive Disorders
|September 23, 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

[Transjugular intrahepatic portosystemic stent shunt (TIPSS) with use of Rösch-Uchida transjugular liver access set--evaluation by CT and its clinical application].

Nihon Igaku Hoshasen Gakkai zasshi. Nippon acta radiologica·1992
Same author

HPC-1 is associated with synaptotagmin and omega-conotoxin receptor.

The Journal of biological chemistry·1992
Same author

Cytohistologic assessment of antitumor effects of intraperitoneal hyperthermic perfusion with mitomycin C for patients with gastric cancer with peritoneal metastasis.

Cancer·1992
Same author

Structure of UvrABC excinuclease-UV-damaged DNA complexes studied by flow linear dichroism. DNA curved by UvrB and UvrC.

FEBS letters·1992
Same author

Quantitative HCV RNA and effect of interferon therapy in chronic hepatitis C.

Digestive diseases and sciences·1992
Same author

[13C] breath test of medium-chain triglycerides and oligosaccharides in neonates.

Acta paediatrica Japonica : Overseas edition·1992

Complement-activated oligodendroglia (CAOs) may be early targets for amyloid-beta deposits. Damaged myelinated axons containing amyloid precursor protein are the source of these deposits in neurodegenerative diseases.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Complement-activated oligodendroglia (CAOs) are implicated in complement-mediated damage.
  • Oligodendroglia are crucial for myelin maintenance in the central nervous system.
  • Amyloid deposits are a hallmark of several neurodegenerative diseases.

Purpose of the Study:

  • To investigate the relationship between CAOs and amyloid deposits in Parkinson's disease, diffuse Lewy body disease, and pallido-nigro-luysial atrophy.
  • To determine the origin of amyloid-beta (A beta) and its association with oligodendroglia.

Main Methods:

  • Immunohistochemistry using anti-C4d and anti-beta-amyloid protein (anti-A beta) antibodies.
  • Examination of parietal lobe tissue from patients with specific neurodegenerative diseases.

Related Experiment Videos

  • Immunoelectron microscopy to visualize cellular and subcellular relationships.

    • Main Results:

    • Numerous CAOs were identified by anti-C4d staining in all patient brains.
    • Amyloid deposits (senile plaques) were found and frequently associated with myelinated axons of CAOs.
    • Amyloid-beta deposits were observed within C4d-positive oligodendroglial cell bodies, suggesting CAOs as potential sites of initial A beta accumulation.

    Conclusions:

    • Damaged myelinated axons, accumulating amyloid precursor protein, are identified as the source of A beta.
    • CAOs are proposed as initial targets for amyloid-beta deposition, contributing to senile plaque formation.
    • These findings offer insights into the early pathological mechanisms in neurodegenerative conditions involving amyloid.