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

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

9.2K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
9.2K
Amyloid Fibrils03:03

Amyloid Fibrils

7.0K
7.0K
Amyloid Fibrils03:03

Amyloid Fibrils

13.2K
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,...
13.2K
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

1.3K
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
1.3K
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

11
Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
11
Pharmacogenomics: Identification of New Drug Targets01:29

Pharmacogenomics: Identification of New Drug Targets

108
Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...
108

You might also read

Related Articles

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

Sort by
Same author

A fragment of 12S seed storage protein of Arabidopsis forms twisted cross beta-sheet rich amyloid fibrils.

International journal of biological macromolecules·2026
Same author

Cardiac phenotype in hereditary transthyretin amyloidosis: correlations between fibril types and 99mTc-DPD uptake.

Scientific reports·2026
Same author

Lysozyme as an amyloid fibril protein together with transthyretin in the ligamentum flavum in association with lumbar spinal stenosis.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis·2026
Same author

Assessment of the biochemical basis underlying the resistance against systemic amyloidosis.

Scientific reports·2026
Same author

Interactions between amyloid fibril proteins.

Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis·2025
Same author

Bri2 BRICHOS domain inhibits IAPP amyloid formation and improves beta cell function in stem cell-derived islets under metabolic stress.

Diabetologia·2025

Related Experiment Video

Updated: Apr 21, 2026

Imaging Amyloid Tissues Stained with Luminescent Conjugated Oligothiophenes by Hyperspectral Confocal Microscopy and Fluorescence Lifetime Imaging
10:04

Imaging Amyloid Tissues Stained with Luminescent Conjugated Oligothiophenes by Hyperspectral Confocal Microscopy and Fluorescence Lifetime Imaging

Published on: October 20, 2017

14.3K

AA amyloidosis: pathogenesis and targeted therapy.

Gunilla T Westermark1, Marcus Fändrich, Per Westermark

  • 1Department of Medical Cell Biology, Uppsala University, 75123 Uppsala, Sweden;

Annual Review of Pathology
|November 12, 2014
PubMed
Summary

AA amyloidosis involves protein misfolding and aggregation into amyloid fibrils, often stemming from chronic inflammation and elevated serum amyloid A (SAA). Recent research offers promising therapeutic strategies for this condition.

Keywords:
acute phasefibrilrheumatoid arthritisserum amyloid Astrainstoxic oligomer

More Related Videos

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease
06:52

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Published on: July 6, 2019

9.8K
Selection of Aptamers for Amyloid β-Protein, the Causative Agent of Alzheimer's Disease
15:23

Selection of Aptamers for Amyloid β-Protein, the Causative Agent of Alzheimer's Disease

Published on: May 13, 2010

20.0K

Related Experiment Videos

Last Updated: Apr 21, 2026

Imaging Amyloid Tissues Stained with Luminescent Conjugated Oligothiophenes by Hyperspectral Confocal Microscopy and Fluorescence Lifetime Imaging
10:04

Imaging Amyloid Tissues Stained with Luminescent Conjugated Oligothiophenes by Hyperspectral Confocal Microscopy and Fluorescence Lifetime Imaging

Published on: October 20, 2017

14.3K
Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease
06:52

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Published on: July 6, 2019

9.8K
Selection of Aptamers for Amyloid β-Protein, the Causative Agent of Alzheimer's Disease
15:23

Selection of Aptamers for Amyloid β-Protein, the Causative Agent of Alzheimer's Disease

Published on: May 13, 2010

20.0K

Area of Science:

  • Biochemistry
  • Immunology
  • Pathology

Background:

  • Protein misfolding and aggregation into amyloid fibrils are key to amyloid formation.
  • AA amyloidosis is linked to chronic inflammation, cytokine expression (e.g., interleukin 6), and serum amyloid A (SAA) overproduction.
  • Amyloid fibrils are characterized by β-sheet structures resistant to degradation.

Purpose of the Study:

  • To review current knowledge on the pathogenesis of AA amyloidosis.
  • To summarize recent advancements in understanding amyloid fibril composition and formation.
  • To highlight emerging therapeutic approaches for AA amyloidosis.

Main Methods:

  • Literature review of recent studies on protein misfolding and amyloidosis.
  • Analysis of the role of cytokines and serum amyloid A in disease development.
  • Examination of the structural properties of amyloid fibrils.

Main Results:

  • Amyloid formation involves increased β-sheet structures and nucleation-dependent fibril generation.
  • Elevated serum amyloid A due to inflammation leads to amyloid deposition in AA amyloidosis.
  • Understanding pathogenesis has paved the way for novel therapeutic strategies.

Conclusions:

  • AA amyloidosis is a consequence of long-standing inflammatory diseases.
  • Despite being considered intractable, AA amyloidosis shows promise for treatment due to improved understanding.
  • Further research into fibril composition and pathogenesis is crucial for developing effective therapies.