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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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Alzheimer's Disease: Overview01:26

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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...
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Related Experiment Video

Updated: Jul 9, 2025

Rapid Generation of Amyloid from Native Proteins In vitro
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Rapid Generation of Amyloid from Native Proteins In vitro

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Once upon a time, the Amyloid Cascade Hypothesis.

Alberto Granzotto1, Stefano L Sensi2

  • 1Center for Advanced Studies and Technology - CAST, University G. d'Annunzio of Chieti-Pescara, Chieti, Italy; Department of Neuroscience, Imaging, and Clinical Sciences, University G. d'Annunzio of Chieti-Pescara, Chieti, Italy.

Ageing Research Reviews
|December 8, 2023
PubMed
Summary

Recent Alzheimer's disease (AD) drug trials targeting amyloid-beta (Aβ) showed minimal real-world benefits, questioning the Amyloid Cascade Hypothesis (ACH). Further research must consider AD's complexity beyond this single target.

Keywords:
AducanumabAlzheimer's diseaseDementiaDonanemabLecanemabNeurodegeneration

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Area of Science:

  • Neurology
  • Pharmacology
  • Biochemistry

Background:

  • Recent clinical trials investigated monoclonal antibodies targeting amyloid-beta (Aβ) for Alzheimer's disease (AD).
  • These therapies aimed to modify AD progression, aligning with the Amyloid Cascade Hypothesis (ACH).
  • Initial results showed mixed outcomes, prompting re-evaluation of current therapeutic strategies.

Purpose of the Study:

  • To critically analyze findings from recent monoclonal antibody trials in AD.
  • To discuss overlooked data and limitations of the Amyloid Cascade Hypothesis (ACH).
  • To advocate for a more comprehensive research approach to Alzheimer's disease.

Main Methods:

  • Review and interpretation of published data from recent AD clinical trials.
  • Critical analysis of the Amyloid Cascade Hypothesis (ACH) in light of trial outcomes.
  • Discussion of multifactorial aspects of Alzheimer's disease pathology.

Main Results:

  • While some neurocognitive test scores improved, significant real-world clinical benefits were limited.
  • Trial results raise questions about the exclusive validity of the Amyloid Cascade Hypothesis (ACH).
  • Overlooked trial data suggests Aβ targeting alone may be insufficient for substantial AD treatment.

Conclusions:

  • Alzheimer's disease is a complex, multifactorial condition requiring broader research perspectives.
  • The Amyloid Cascade Hypothesis (ACH) may be an oversimplification of AD pathogenesis.
  • Future AD research should explore diverse therapeutic targets beyond amyloid-beta.