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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...

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Multicenter cohort analysis of cardiac amyloidosis patients treated with heart transplant.

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Multifaceted effects of N-glycosylation on amyloidogenic κ light chains in AL amyloidosis.

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Related Experiment Video

Updated: May 15, 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

Light chain amyloidosis 2012: a new era.

Moshe E Gatt1, Giovanni Palladini

  • 1Department of Haematology, Hadassah Hebrew University Medical Centre, Jerusalem, Israel. rmoshg@hadassah.org.il

British Journal of Haematology
|January 9, 2013
PubMed
Summary

Autologous stem cell transplantation improves survival for AL amyloidosis patients but has high toxicity. Novel drug combinations offer better remission and survival rates, even for high-risk patients.

Area of Science:

  • Hematology
  • Oncology
  • Internal Medicine

Background:

  • AL amyloidosis with multi-organ involvement, especially cardiac, historically indicates a poor prognosis.
  • Autologous stem cell transplantation (ASCT) offers prolonged survival but carries significant toxicity, limiting its use in high-risk patients.
  • Careful patient selection for ASCT reduces toxicity but restricts treatment applicability.

Purpose of the Study:

  • To review the state-of-the-art treatment for AL amyloidosis as of 2012.
  • To highlight recent advancements in managing AL amyloidosis.
  • To discuss novel therapeutic regimens and their impact on patient outcomes.

Main Methods:

  • Review of recent literature on AL amyloidosis treatment.
  • Analysis of outcomes with novel drug combinations including immunomodulatory drugs and proteasome inhibitors.

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From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia

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Last Updated: May 15, 2026

Imaging Amyloid Tissues Stained with Luminescent Conjugated Oligothiophenes by Hyperspectral Confocal Microscopy and Fluorescence Lifetime Imaging
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From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia

Published on: October 19, 2014

  • Evaluation of treatment efficacy in high-risk patient populations.

    • Main Results:

    • Novel drug combinations (thalidomide, lenalidomide, bortezomib) with dexamethasone and alkylating agents show promising results.
    • High remission rates and improved event-free and overall survival are achievable.
    • These regimens benefit a significant proportion of high-risk patients with poor prognosis.

    Conclusions:

    • Newer therapeutic strategies have significantly improved AL amyloidosis management.
    • Effective treatment options are now available for a broader range of patients, including those at high risk.
    • Continued research is essential for further optimizing AL amyloidosis treatment regimens.