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

521
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...
521

You might also read

Related Articles

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

Sort by
Same author

Carboxyl Surface Modification Attenuates Polystyrene- but Not Poly(methyl methacrylate) Nanoplastic-Induced Gut Dysbiosis in Zebrafish Larvae.

Environment & health (Washington, D.C.)·2026
Same author

BRICHOS-Biased Inhibition Contributes to Aβ42 Dominance in Parenchymal Plaques Despite Higher Aβ40 Abundance and Coaggregation Capability.

Biomacromolecules·2026
Same author

Coaggregation with Aβ Drives β-Sheet Formation in tau Microtubule-Binding Repeats.

Biomacromolecules·2026
Same author

Quantifying electrostatic control of docking and binding energetics in functional Cx36 gap junctions.

Communications biology·2026
Same author

From Microbial Dysbiosis to Host Pathogenesis: Unraveling the Gut Microbiome's Role in Environmental Toxicology.

Environment & health (Washington, D.C.)·2026
Same author

Nanoplastics and Neurodegeneration: A Roadmap From Mechanism to Causation.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026

Related Experiment Video

Updated: Jul 19, 2025

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
04:41

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

23.3K

Spike Protein Fragments Promote Alzheimer's Amyloidogenesis.

Sujian Cao1, Zhiyuan Song2, Jinyu Rong3

  • 1Nanomedicine Center, The Great Bay Area National Institute for Nanotechnology Innovation, 136 Kaiyuan Avenue, Guangzhou, 510700, China.

ACS Applied Materials & Interfaces
|August 16, 2023
PubMed
Summary

The SARS-CoV-2 spike protein fragment promotes Alzheimer's disease (AD) pathology by enhancing amyloid-beta aggregation. This finding suggests viral infections may contribute to neurodegeneration and Long Covid complications.

Keywords:
Alzheimer’s diseaseSARS-CoV-2amyloid βspike proteinvirus

More Related Videos

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
07:55

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP

Published on: October 17, 2015

11.9K
Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease
06:52

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Published on: July 6, 2019

9.3K

Related Experiment Videos

Last Updated: Jul 19, 2025

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
04:41

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

23.3K
Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
07:55

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP

Published on: October 17, 2015

11.9K
Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease
06:52

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Published on: July 6, 2019

9.3K

Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is a leading cause of dementia, primarily linked to amyloid-beta (Aβ) aggregation.
  • The role of viral infections, including SARS-CoV-2, in AD pathogenesis is not well understood.
  • COVID-19's long-term neurological effects, such as Long Covid, require further investigation.

Purpose of the Study:

  • To investigate the amyloidogenic potential of a SARS-CoV-2 spike protein fragment.
  • To determine if this viral peptide fragment interacts with and promotes Aβ aggregation.
  • To explore the potential link between SARS-CoV-2 infection and Alzheimer's disease.

Main Methods:

  • In vitro and in silico methods were used to assess the amyloidogenic properties of the SARS-CoV-2 peptide fragment.
  • Binding affinity between the viral peptide and Aβ segments was analyzed.
  • Zebrafish embryos were used to evaluate the toxicity of the peptide fragment.

Main Results:

  • A short fragment of the SARS-CoV-2 spike protein (1058HGVVFLHVTYV1068) was identified as amyloidogenic.
  • The viral peptide fragment demonstrated high binding propensity to Aβ, promoting its aggregation and toxicity in vitro and in silico.
  • Exposure to the peptide fragment retarded zebrafish embryo hatching and survival.

Conclusions:

  • SARS-CoV-2 infection may contribute to Alzheimer's disease pathogenesis.
  • The interaction between viral proteins and Aβ aggregation presents a novel mechanism for neurodegeneration.
  • Understanding these interactions is crucial for addressing Long Covid and developing therapeutic strategies.