Related Experiment Video
Updated: Jul 4, 2026
05:48
Rapid Generation of Amyloid from Native Proteins In vitro
Published on: December 5, 2013
[Amyloidosis AA].
Katia Stankovic1, Gilles Grateau
1Service de Médecine Interne, Hôpital Tenon, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris Cedex 20, France.
Nephrologie & Therapeutique
|June 3, 2008
Summary
Amyloid-associated (AA) amyloidosis, often caused by inflammatory conditions like rheumatoid arthritis, is decreasing in Western countries. Diagnosis involves monitoring kidney function and acute phase reactants, with treatments targeting inflammation.
Area of Science:
- Rheumatology
- Nephrology
- Oncology
Context:
- Amyloidosis encompasses immunoglobulinic (AL), hereditary, and amyloid-associated (AA) types.
- AA amyloidosis is primarily linked to chronic inflammatory disorders such as rheumatoid arthritis and autoimmune conditions.
- Tumors like Castleman's disease can also precipitate AA amyloidosis.
Purpose:
- To summarize current understanding of amyloid-associated (AA) amyloidosis, its causes, diagnosis, and prognosis.
- To highlight the role of inflammatory disorders and acute phase response in AA amyloidosis development.
- To discuss diagnostic strategies, including monitoring renal function and immunohistochemistry, and current therapeutic approaches.
Summary:
- AA amyloidosis incidence is declining in Western nations, with inflammatory diseases being primary drivers.
- A sustained acute phase response, indicated by serum amyloid A (SAA) protein levels, is crucial for AA amyloidosis development.
- Nephropathy is the most common clinical presentation, necessitating regular monitoring of proteinuria and creatinine.
- Complete surgical removal of causative tumors can lead to amyloid regression.
- Genetic factors are increasingly recognized as contributors.
- Diagnosis requires comprehensive clinical and pathological data, distinguishing it from other amyloidosis types.
- Poor prognosis is associated with renal failure and malnutrition due to gut involvement.
- Current treatments focus on reducing inflammation, with novel therapies targeting amyloid deposition under development.
Impact:
- Provides a concise overview of AA amyloidosis for clinicians and researchers.
- Emphasizes the importance of early detection and management of underlying inflammatory conditions.
- Informs therapeutic strategies, focusing on anti-inflammatory approaches and future drug development for amyloidosis.
Related Concept Videos
03:03Amyloid Fibrils
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
03:03Amyloid Fibrils
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
01:23Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
01:22Myasthenia Gravis ll: Pathophysiology
The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...