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

Complement component C5 is not involved in scrapie pathogenesis.

Neil A Mabbott1, Moira E Bruce

  • 1Institute for Animal Health, Neuropathoqenesis Unit, Ogston Building, West Mains Road, Edinburgh EH9 3JF, Scotland, UK. neil.mabbott@bbsrc.ac.uk

Immunobiology
|December 1, 2004
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

The genome sequence of the nematode <i>Ostertagia ostertagi</i> (Stiles, 1892) (Rhabditida, Trichostrongylidae).

Wellcome open research·2026
Same author

TREM2 supports neuronal protection and microglial reactivity without an effect on misfolded protein deposition in chronic neurodegenerative prion disease.

Frontiers in neuroscience·2025
Same author

Non-neuronal brain biology and its relevance to animal welfare.

Neuroscience and biobehavioral reviews·2025
Same author

Acute LPS exposure enhances susceptibility to peripheral prion infection.

Scientific reports·2025
Same author

Systematic review and meta-analysis of COVID-19 mRNA vaccine effectiveness against hospitalizations in adults.

Immunotherapy advances·2024
Same author

The effect of a dominant kinase-dead Csf1r mutation associated with adult-onset leukoencephalopathy on brain development and neuropathology.

Neurobiology of disease·2024
Same journal

ST2-mediated ERK/JNK/P38/NF-κB signaling: a target of Biminkang mixture in minimal persistent inflammation of allergic rhinitis.

Immunobiology·2026
Same journal

Chronic stress promotes colorectal cancer progression by inducing M2 macrophage polarization and activating the CCL2-CCR2 axis.

Immunobiology·2026
Same journal

Spatial-cellular resolution analysis of ferroptosis-associated immune microenvironment heterogeneity in osteoarthritic cartilage.

Immunobiology·2026
Same journal

Exploring therapeutic targets for neuroinflammation in sepsis-associated encephalopathy: a combined network pharmacology and bioinformatics approach.

Immunobiology·2026
Same journal

Potential correlation assessment identified by a genome-wide association study using induced pluripotent stem cells from patients with IgAN.

Immunobiology·2026
Same journal

MicroRNA-5011-5p attenuates LPS-induced inflammatory damage in periodontal ligament cells by targeting KLF6: an in vitro study.

Immunobiology·2026
See all related articles

The membrane attack complex (MAC) is not involved in transmissible spongiform encephalopathy (TSE) pathogenesis. Studies show C5-deficient mice infected with scrapie exhibit similar disease progression and neuropathology to C5-sufficient mice.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Transmissible spongiform encephalopathies (TSEs) involve prion protein accumulation and neurodegeneration.
  • The complement system, specifically the membrane attack complex (MAC, C5b-C9), is implicated in neurodegenerative diseases.
  • MAC has been observed on neurons in TSE patients, suggesting a role in neuropathology.

Purpose of the Study:

  • To investigate the role of the MAC in TSE pathogenesis.
  • To determine if C5, a key component of MAC formation, influences scrapie progression and neuropathology.

Main Methods:

  • Comparison of scrapie pathogenesis in C5-deficient mice and C5-sufficient control mice.
  • Monitoring of clinical signs and neuropathological severity in both groups.

Related Experiment Videos

Main Results:

  • C5-deficient mice developed clinical scrapie with incubation periods comparable to C5-sufficient mice.
  • Neuropathological severity was not significantly different between C5-deficient and C5-sufficient mice.
  • These findings indicate no involvement of C5 or MAC in TSE pathogenesis.

Conclusions:

  • The complement system component C5 and the membrane attack complex (MAC) do not play a significant role in the pathogenesis of transmissible spongiform encephalopathies.
  • These results challenge the hypothesis that complement-mediated cell lysis contributes to TSE neuropathology.