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

[Amyloidosis and aging].

Nagi Mimassi1, Pierre Youinou, Yvon-Louis Pennec

  • 1Service de Rhumatologie, Centre Hospitalier Universitaire, 29609 Brest Cedex, France.

Annales De Medecine Interne
|December 18, 2002
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

Uric acid increases IL-1β secretion and Caspase-1 activation in PBMCs of Behçet's disease patients: The in vitro immunomodulatory effect of xanthine oxidase inhibitor Allopurinol.

International immunopharmacology·2020
Same author

Increased IL-1β levels are associated with an imbalance of "oxidant/antioxidant" status during Behçet's disease.

European cytokine network·2018
Same author

Interferon-β inhibits inflammatory responses mediators via suppression of iNOS signaling pathway in PBMCs from patients with primary Sjögren's syndrome.

Inflammopharmacology·2018
Same author

Cardamonin inhibits pro-inflammatory cytokine production and suppresses NO pathway in PBMCs from patients with primary Sjögren's syndrome.

Immunopharmacology and immunotoxicology·2018
Same author

Human regulatory B cells control the T<sub>FH</sub> cell response.

The Journal of allergy and clinical immunology·2016
Same author

CD5 expression promotes IL-10 production through activation of the MAPK/Erk pathway and upregulation of TRPC1 channels in B lymphocytes.

Cellular & molecular immunology·2016

Amyloidosis involves protein deposits in the body. Age-related forms can be systemic, like senile systemic amyloidosis from transthyretin, or localized, often without significant clinical impact except in specific diseases.

Area of Science:

  • Pathology
  • Gerontology
  • Biochemistry

Context:

  • Amyloidosis encompasses diverse extracellular protein deposition disorders.
  • Age-related amyloidosis presents as systemic or localized forms.
  • Understanding the clinical significance of localized amyloidosis remains an ongoing challenge.

Purpose:

  • To differentiate between systemic and localized age-related amyloidosis.
  • To identify the precursors of amyloid fibrils in various forms of amyloidosis.
  • To explore the clinical relevance of localized amyloid deposits.

Summary:

  • Systemic age-related amyloidosis includes senile systemic amyloidosis (transthyretin-derived) and AL amyloidosis (myeloma-associated).
  • Localized amyloidosis involves tissue-specific synthesis of fibril precursors.

Related Experiment Videos

  • Most localized forms are clinically silent, barring associations with Alzheimer's disease and type 2 diabetes mellitus.
  • Impact:

    • Clarifies the classification and origins of age-related amyloidosis.
    • Highlights the differential clinical impact of systemic versus localized amyloidosis.
    • Identifies areas requiring further research, such as aortic, seminal vesicle, endocrine, and articular amyloidosis.