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 Concept Videos

Amyloid Fibrils03:03

Amyloid 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 Fibrils03:03

Amyloid 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...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer 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...
Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of fluid...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia 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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The EKiTE network (epidemiology in kidney transplantation - a European validated database): an initiative epidemiological and translational European collaborative research.

BMC nephrology·2019
Same author

Cytomegalovirus colitis.

Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia·2011
Same author

[Preservation by pulsatile perfusion machine: the initial experience].

Actas urologicas espanolas·1999
Same author

[An immunohistochemical study of chronic otitis media].

Acta otorrinolaringologica espanola·1991
Same author

[Systematic study with immunofluorescence of autopsy kidneys].

Revista clinica espanola·1986
Same author

[Importance of visualization and quantification of the gastrin-secreting G cells of the antrum].

Revista espanola de las enfermedades del aparato digestivo·1982

Related Experiment Video

Updated: Jul 6, 2026

Rapid Generation of Amyloid from Native Proteins In vitro
05:48

Rapid Generation of Amyloid from Native Proteins In vitro

Published on: December 5, 2013

[Systemic AA amyloidosis induced by benign neoplasms].

O Bestard Matamoros1, R Poveda Monje, M Ibernon Vilaró

  • 1Hospital de Bellvitge, Hospitalet de Llobregat, Barcelona. 35830obm@comb.es

Nefrologia : Publicacion Oficial De La Sociedad Espanola Nefrologia
|March 14, 2008
PubMed
Summary

AA amyloidosis can result from benign neoplasms, not just chronic inflammation. Early diagnosis and treatment of these tumors may lead to regression of AA amyloidosis.

More Related Videos

Performing and Processing FNA of Anterior Fat Pad for Amyloid
09:41

Performing and Processing FNA of Anterior Fat Pad for Amyloid

Published on: October 30, 2010

Related Experiment Videos

Last Updated: Jul 6, 2026

Rapid Generation of Amyloid from Native Proteins In vitro
05:48

Rapid Generation of Amyloid from Native Proteins In vitro

Published on: December 5, 2013

Performing and Processing FNA of Anterior Fat Pad for Amyloid
09:41

Performing and Processing FNA of Anterior Fat Pad for Amyloid

Published on: October 30, 2010

Area of Science:

  • Nephrology
  • Oncology
  • Immunology

Background:

  • Amyloidosis is a systemic disorder involving the deposition of toxic protein aggregates.
  • AA amyloidosis, a common type, results from serum amyloid A (SAA) protein fragments and often complicates chronic inflammatory diseases.
  • While less common, benign neoplasms can also lead to AA amyloidosis.

Observation:

  • Two cases of AA amyloidosis secondary to benign neoplasms are presented.
  • Case 1: A hepatic adenoma led to AA amyloidosis with nephrotic syndrome, resulting in renal failure and subsequent kidney transplantation.
  • Case 2: Castleman's disease caused AA amyloidosis and nephrotic syndrome, leading to renal failure and kidney transplantation.

Findings:

  • Benign tumors, such as hepatic adenoma and Castleman's disease, can be etiological causes of AA amyloidosis.
  • AA amyloidosis presentation can include primary kidney involvement, such as nephrotic syndrome.
  • Despite treatment and transplantation, progressive renal failure can occur.

Implications:

  • Benign neoplasms should be considered as potential causes of AA amyloidosis.
  • Early diagnosis and treatment of associated neoplasms may facilitate regression of AA amyloidosis.
  • This highlights the importance of a comprehensive etiological investigation in amyloidosis cases.