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Amyloid Fibrils03:03

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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. 
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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...
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Related Experiment Video

Updated: Apr 27, 2026

Imaging Amyloid Tissues Stained with Luminescent Conjugated Oligothiophenes by Hyperspectral Confocal Microscopy and Fluorescence Lifetime Imaging
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[Classification of amyloidosis].

Yohei Misumi1, Yukio Ando

  • 1Department of Neurology, Faculty of Life Sciences, Kumamoto University.

Brain and Nerve = Shinkei Kenkyu No Shinpo
|July 8, 2014
PubMed
Summary
This summary is machine-generated.

Amyloidoses are protein misfolding diseases where proteins form amyloid fibrils. Early diagnosis and precise classification are crucial for effective treatment as many forms are now treatable.

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Area of Science:

  • Protein conformational diseases
  • Extracellular matrix deposition
  • Protein misfolding disorders

Context:

  • Amyloidoses involve the formation of insoluble amyloid fibrils from soluble precursor proteins.
  • Classification includes localized or systemic deposition and is based on precursor protein type.
  • Currently, 27 different amyloid precursor proteins are recognized.

Purpose:

  • To review the classification, diagnosis, and treatment of amyloidoses.
  • To highlight the importance of early diagnosis and precise classification for improved outcomes.
  • To underscore recent advancements in amyloidosis treatment strategies.

Summary:

  • Amyloidoses are classified by deposition site (localized/systemic) and precursor protein type.
  • Diagnosis relies on histopathology (Congo red, electron microscopy) and classification via immunohistochemistry, proteomics, and gene analysis.
  • Key systemic types include light-chain, reactive amyloid A, β2-microglobulin, and hereditary transthyretin amyloidosis.

Impact:

  • Improved understanding of amyloidosis heterogeneity.
  • Facilitates precise disease classification for targeted therapy.
  • Emphasizes the growing treatability of various amyloidosis forms.
  • Highlights the critical need for early diagnosis and intervention.