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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...
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...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...

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Related Experiment Video

Updated: May 23, 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

[AL amyloidosis].

Klára Gadó1, Gyula Domján

  • 1Semmelweis Egyetem, Általános Orvostudományi Kar I. Belgyógyászati Klinika Budapest Korányi Sándor u. gadok@freemail.hu

Orvosi Hetilap
|April 5, 2012
PubMed
Summary
This summary is machine-generated.

AL amyloidosis involves malignant plasma cells producing proteins that damage organs. Early diagnosis and treatment, including chemotherapy and stem cell transplants, are crucial for managing this rare disease.

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Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis
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Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis

Published on: June 9, 2018

Related Experiment Videos

Last Updated: May 23, 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

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis
06:33

Genetic Analysis of Hereditary Transthyretin Ala97Ser Related Amyloidosis

Published on: June 9, 2018

Area of Science:

  • Hematology
  • Oncology
  • Nephrology

Background:

  • AL amyloidosis is a systemic plasma cell dyscrasia characterized by the deposition of abnormal immunoglobulin light chains.
  • These deposits lead to organ dysfunction, particularly affecting the heart and kidneys.
  • It is associated with monoclonal gammopathies and B-cell malignancies.

Purpose of the Study:

  • To review the diagnosis and current therapeutic strategies for AL amyloidosis.
  • To emphasize the importance of early detection and risk stratification in treatment decisions.
  • To highlight the evolving treatment landscape with novel agents and stem cell transplantation.

Main Methods:

  • Diagnosis relies on histological confirmation and identification of the specific amyloidogenic protein.
  • Treatment strategies include high-dose chemotherapy with autologous stem cell transplantation for eligible patients.
  • Novel agents like thalidomide, lenalidomide, and bortezomib are used for transplant-ineligible patients or as alternatives.

Main Results:

  • Eradication of the malignant plasma cell clone is the primary therapeutic goal.
  • Advanced organ damage, especially cardiac failure, can limit treatment effectiveness.
  • Significant advancements in therapeutic options have improved management possibilities.

Conclusions:

  • AL amyloidosis requires a multidisciplinary approach with careful risk assessment before initiating treatment.
  • Prompt diagnosis and treatment initiation are critical for improving outcomes.
  • Specialized centers are vital for clinical trials and advancing the care of this orphan disease.