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Related Concept Videos

Amyloid Fibrils03:03

Amyloid Fibrils

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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. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining,...
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TGF - β Signaling Pathway01:16

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Related Experiment Video

Updated: Jul 29, 2025

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis
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A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis

Published on: May 22, 2018

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Amyloid-β is a cytokine.

Donald F Weaver1

  • 1Krembil Research Institute, University Health Network, University of Toronto, Toronto, Ontario, Canada.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|May 25, 2023
PubMed
Summary

Amyloid-beta (Aβ) is reclassified as a cytokine, a signaling molecule crucial for immune responses. This finding helps unify Alzheimer's disease (AD) theories, linking amyloid plaques and neuroinflammation.

Area of Science:

  • Neuroscience
  • Immunology
  • Biochemistry

Background:

  • The physiological role of amyloid-beta (Aβ) in humans is not fully understood.
  • Aβ's specific function in Alzheimer's disease (AD) pathogenesis remains a subject of debate.

Purpose of the Study:

  • To critically evaluate the existing literature on amyloid-beta (Aβ).
  • To determine the precise classification and physiological role of Aβ.
  • To integrate disparate hypotheses regarding Alzheimer's disease (AD) mechanisms.

Main Methods:

  • A comprehensive review of scientific literature was conducted.
  • Thirty characteristic structural and functional properties of cytokines were identified.
  • Aβ's properties were systematically compared against the defined cytokine characteristics.
Keywords:
Alzheimer's diseaseamyloid-betaautoimmunechemokinecytokinedementia

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Main Results:

  • Amyloid-beta (Aβ) was found to possess all 30 identified properties of cytokines.
  • This comprehensive analysis provides systematic justification for classifying Aβ as a cytokine.
  • The classification of Aβ as a cytokine offers a unified framework for understanding AD.

Conclusions:

  • Amyloid-beta (Aβ) functions as a cytokine.
  • This reclassification bridges the amyloid hypothesis and neuroinflammation hypothesis of Alzheimer's disease (AD).
  • Understanding Aβ as a cytokine provides new avenues for AD research and therapeutic strategies.