Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Amyloid Fibrils03:03

Amyloid Fibrils

9.6K
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,...
9.6K
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

498
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...
498

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Glial cytokine modulation improves sleep and circadian disruption in female SAA knock-in mice of Alzheimer's-related pathology.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same author

Dim light at night impacts circadian rhythms and Alzheimer's disease-like neuroinflammation and neuropathology in humanized APP SAA knock-in mice.

Sleep·2026
Same author

Circadian rhythm of amyloid-β in the olfactory bulb and cerebellum of wild-type and APPxPS1 knock-in mice indicates a loss of rhythmicity in regions more vulnerable to amyloid pathology.

Biogerontology·2025
Same author

Dim light at night impacts circadian rhythms and Alzheimer's disease-like neuroinflammation and neuropathology in humanized APP SAA knock-in mice.

bioRxiv : the preprint server for biology·2025
Same author

Chronic Sleep Fragmentation Differentially Affects Alzheimer's Disease Pathology in Male and Female APP<sup>SAA</sup> Knock-in Mice.

Journal of inflammation research·2025
Same author

Interactions between daily sleep-wake rhythms, γ-secretase, and amyloid-β peptide pathology point to complex underlying relationships.

Biochimica et biophysica acta. Molecular basis of disease·2025

Related Experiment Video

Updated: Jul 11, 2025

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain
10:08

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain

Published on: August 28, 2012

11.8K

The amyloid-β peptide: Guilty as charged?

M Paul Murphy1, Valeria A Buzinova1, Carrie E Johnson1

  • 1Department of Molecular and Cellular Biochemistry and the Sanders-Brown Center on Aging University of Kentucky, 789 S. Limestone Street, Lexington, KY 40536, USA.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|November 7, 2023
PubMed
Summary

Recent Alzheimer's disease therapies targeting amyloid-beta (Aβ) show modest efficacy in slowing progression. However, the complete removal of Aβ does not halt the disease, posing a puzzle for the amyloid cascade hypothesis.

Keywords:
APPAmyloidFibrilOligomerPlaquesβ-Amyloid precursor protein

More Related Videos

Visualization of Amyloid &#946; Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
09:31

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

10.7K
Detecting Amyloid-&#946; Accumulation via Immunofluorescent Staining in a Mouse Model of Alzheimer's Disease
08:25

Detecting Amyloid-β Accumulation via Immunofluorescent Staining in a Mouse Model of Alzheimer's Disease

Published on: April 19, 2021

3.3K

Related Experiment Videos

Last Updated: Jul 11, 2025

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain
10:08

Purification and Aggregation of the Amyloid Precursor Protein Intracellular Domain

Published on: August 28, 2012

11.8K
Visualization of Amyloid &#946; Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
09:31

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

10.7K
Detecting Amyloid-&#946; Accumulation via Immunofluorescent Staining in a Mouse Model of Alzheimer's Disease
08:25

Detecting Amyloid-β Accumulation via Immunofluorescent Staining in a Mouse Model of Alzheimer's Disease

Published on: April 19, 2021

3.3K

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • The Alzheimer's disease (AD) field has experienced limited progress in developing disease-modifying therapies until recently.
  • The amyloid cascade hypothesis posits that amyloid-beta (Aβ) accumulation is a primary driver of AD pathogenesis.
  • Monoclonal antibodies targeting Aβ have emerged as a potential therapeutic strategy.

Purpose of the Study:

  • To review the recent advancements and controversies surrounding anti-amyloid-beta (Aβ) therapeutics in Alzheimer's disease.
  • To evaluate the efficacy of Aβ-targeting therapies in clinical trials.
  • To address the discrepancy between Aβ removal and complete disease halting.

Main Methods:

  • Analysis of recent clinical trial outcomes for monoclonal antibodies targeting Aβ.
  • Review of scientific literature concerning the amyloid cascade hypothesis and AD pathogenesis.
  • Discussion of the implications of current therapeutic results for understanding AD.

Main Results:

  • Several monoclonal antibodies targeting Aβ have demonstrated modest efficacy in slowing Alzheimer's disease progression.
  • Multiple anti-Aβ therapeutics are nearing or have received regulatory approval.
  • Despite Aβ removal, the disease progression is not entirely halted, indicating a complex disease mechanism.

Conclusions:

  • Targeting amyloid-beta for removal represents a significant, albeit not complete, therapeutic advance in Alzheimer's disease.
  • The partial efficacy of Aβ-clearing therapies challenges a simplistic view of the amyloid cascade hypothesis.
  • Further research is needed to elucidate the precise role of Aβ and identify additional therapeutic targets for AD.