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

Dysregulation of complement at the synapse in P301S mice and human tauopathies.

Acta neuropathologica communications·2026
Same author

A synonymous SLC2A1 variant causes familial epilepsy and paroxysmal exercise-induced dyskinesia by creating aberrant mosaic splicing patterns.

Neurobiology of disease·2026
Same author

From Dish to Trial: Building Translational Models of ALS.

Cells·2026
Same author

Activation of the Lectin Pathway Drives Persistent Complement Dysregulation in Long COVID.

Immunology·2026
Same author

Absence of complement terminal pathway activity in C6-deficient mice prolongs survival in a mouse model of severe malarial infection.

Immunobiology·2025
Same author

CD59, Disulphide-Locked Human C9 and Horse C9 Inhibit Human Membrane Attack Complex Assembly by Similar Mechanisms.

Immunology·2025

Related Experiment Video

Updated: Mar 19, 2026

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines
09:46

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines

Published on: September 21, 2021

5.3K

Complement is activated in progressive multiple sclerosis cortical grey matter lesions.

Lewis M Watkins1, James W Neal2, Sam Loveless3

  • 1Institute of Life Sciences, Swansea University School of Medicine, Swansea, SA2 8PP, UK.

Journal of Neuroinflammation
|June 24, 2016
PubMed
Summary
This summary is machine-generated.

Complement over-activation in the brain

Keywords:
ComplementGrey matter lesionInnate immunityMultiple sclerosisNeurodegeneration

More Related Videos

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

12.2K
An Ex vivo Model of an Oligodendrocyte-directed T-Cell Attack in Acute Brain Slices
06:36

An Ex vivo Model of an Oligodendrocyte-directed T-Cell Attack in Acute Brain Slices

Published on: February 5, 2015

7.6K

Related Experiment Videos

Last Updated: Mar 19, 2026

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines
09:46

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines

Published on: September 21, 2021

5.3K
Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

12.2K
An Ex vivo Model of an Oligodendrocyte-directed T-Cell Attack in Acute Brain Slices
06:36

An Ex vivo Model of an Oligodendrocyte-directed T-Cell Attack in Acute Brain Slices

Published on: February 5, 2015

7.6K

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Multiple sclerosis (MS) symptoms arise from myelin and nerve cell damage in the central nervous system.
  • Neuroinflammation and neurodegeneration drive progressive disability in MS.
  • Understanding grey matter pathology is crucial for MS progression insights.

Purpose of the Study:

  • To investigate complement system expression and activation in progressive MS grey matter.
  • To compare complement activity in MS grey matter with controls.

Main Methods:

  • Immunocytochemistry and in situ hybridization on post-mortem brain tissue from 22 progressive MS cases.
  • Comparison with inflammatory central nervous system disease and non-neurological disease controls.

Main Results:

  • Complement component C1qA and activation fragment C3b were found on neurons and glia in MS grey matter.
  • Increased C1q and Bb deposition in MS cortical lesions indicated complement pathway activation.
  • Elevated membrane attack complex and complement receptor-positive microglia suggest complement over-activation in MS grey matter lesions.

Conclusions:

  • Complement activation occurs in MS cortical grey matter lesions.
  • Over-activation of the complement system may contribute to irreversible MS progression and neurodegeneration.