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

The transmissible spongiform encephalopathies.

C I Lasmézas1

  • 1Commissariat à l'Energie Atomique, Laboratoire de Pathogènes des Prions, Service de Neurovirologie, Direction des Sciences du Vivant/Département de Recherche Médicale, BP 6, 92265 Fontenay-aux-Roses, France.

Revue Scientifique Et Technique (International Office of Epizootics)
|June 10, 2003
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

Tissue distribution of bovine spongiform encephalopathy agent in primates after intravenous or oral infection.

Lancet (London, England)·2004
Same author

The 37-kDa/67-kDa laminin receptor acts as the cell-surface receptor for the cellular prion protein.

The EMBO journal·2001
Same author

Identification of interaction domains of the prion protein with its 37-kDa/67-kDa laminin receptor.

The EMBO journal·2001
Same author

Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt-- Jakob disease: implications for human health.

Proceedings of the National Academy of Sciences of the United States of America·2001
Same author

Diagnosis of bovine spongiform encephalopathy.

Veterinary journal (London, England : 1997)·2001
Same author

Role of spleen macrophages in the clearance of scrapie agent early in pathogenesis.

The Journal of pathology·2000

Transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative diseases with long incubation periods. Research focuses on understanding prion protein (PrP) accumulation and replication for effective TSE risk management.

Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Biochemistry

Background:

  • Transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative diseases.
  • Characterized by long incubation periods and central nervous system lesions.
  • Causative agents, prions, are primarily composed of modified prion protein (PrP).

Purpose of the Study:

  • To present general features of TSEs.
  • To provide a modern understanding of TSE agents and their replication.
  • To discuss advances in PrP accumulation, detection, and risk management.

Main Methods:

  • Literature review and synthesis of current knowledge on TSEs.
  • Analysis of prion protein (PrP) structure and function.
  • Overview of diagnostic and risk management strategies.

Related Experiment Videos

Main Results:

  • Pathological prion protein (PrPSc/PrPRes) accumulates in target organs.
  • TSE pathogenesis involves lymphoid organ replication followed by neuroinvasion.
  • Understanding PrP accumulation and detection is key for risk management.

Conclusions:

  • Despite open questions on TSE aetiology, pathogenesis is increasingly understood.
  • Advances in understanding PrP accumulation provide tools for TSE risk management.
  • Further research into prion replication and detection is crucial.