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

You might also read

Related Articles

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

Sort by
Same author

Biological aging clocks in health and disease.

Nature medicine·2026
Same author

Plasma proteomic signatures of cellular aging predict human disease.

Nature medicine·2026
Same author

Alzheimer's disease biological domain sub-stratification enhances the precision of functional analyses.

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

Mapping cross-domain drivers of Alzheimer's disease risk through integrated network analysis.

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

Plasma proteomics reveals divergent sex-specific senescence and bone biology signatures across neurodegenerative diseases.

bioRxiv : the preprint server for biology·2026
Same author

Taming the "death receptor": translating the first-in-class p75<sup>NTR</sup> modulator LM11A-31 from basic biology, across broad preclinical models, to clinical proof-of-concept.

Journal of translational medicine·2026

Related Experiment Video

Updated: Mar 6, 2026

Correlative Light and Electron Microscopy to Study Microglial Interactions with &#946;-Amyloid Plaques
10:52

Correlative Light and Electron Microscopy to Study Microglial Interactions with β-Amyloid Plaques

Published on: June 1, 2016

12.1K

Microglial complement receptor 3 regulates brain Aβ levels through secreted proteolytic activity.

Eva Czirr1, Nicholas A Castello2, Kira I Mosher1

  • 1Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305.

The Journal of Experimental Medicine
|March 17, 2017
PubMed
Summary

Microglia

More Related Videos

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
09:33

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

8.5K
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

11.2K

Related Experiment Videos

Last Updated: Mar 6, 2026

Correlative Light and Electron Microscopy to Study Microglial Interactions with &#946;-Amyloid Plaques
10:52

Correlative Light and Electron Microscopy to Study Microglial Interactions with β-Amyloid Plaques

Published on: June 1, 2016

12.1K
Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
09:33

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

8.5K
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

11.2K

Area of Science:

  • Neuroscience
  • Immunology
  • Alzheimer's Disease Research

Background:

  • Genetic evidence links microglia and the complement system in Alzheimer's Disease (AD).
  • The role of microglial complement receptor 3 (CR3) in amyloid-beta (Aβ) regulation is not fully understood.

Purpose of the Study:

  • To investigate the novel role of microglial CR3 in soluble Aβ clearance.
  • To explore CR3's impact on Aβ accumulation and degradation in AD models.

Main Methods:

  • Utilized human amyloid precursor protein-transgenic mouse models with CR3 ablation.
  • Examined Aβ levels in cultured microglia and in vivo using microdialysis.
  • Analyzed extracellular Aβ degradation by microglia.

Main Results:

  • CR3 ablation in mice led to decreased, not increased, Aβ accumulation.
  • CR3-deficient microglia showed enhanced extracellular Aβ degradation via secreted enzymes like tissue plasminogen activator.
  • A CR3 modulator reduced soluble Aβ levels and half-life in brain interstitial fluid.

Conclusions:

  • Microglial CR3 limits soluble Aβ clearance from brain interstitial fluid, contrary to expectations.
  • CR3 plays a novel role in brain Aβ metabolism.
  • CR3 represents a potential therapeutic target for Alzheimer's Disease.