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

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

20
Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
20
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

35
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
35
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

28
Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
28

You might also read

Related Articles

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

Sort by
Same author

Myelin antigen-specific effector CD8+ T cells induce chronic CNS autoimmunity in a CD4+ T cell-dependent manner.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same author

Erythrocyte Fragility in Progressive Multiple Sclerosis.

European journal of neurology·2026
Same author

Epstein-Barr Virus Antibodies to Differentiate Multiple Sclerosis From Other Neuroinflammatory Diseases.

JAMA neurology·2026
Same author

The functional role of glial cells in the pathologic brain as reviewed by Alois Alzheimer in 1910.

Molecular neurodegeneration·2026
Same author

Characteristic patterns of complement deposition in NMOSD, MOGAD, and MS.

Acta neuropathologica·2026
Same author

The dynamics of brain T cell populations during the course of rasmussen encephalitis: from expansion to exhaustion.

Journal of neuroinflammation·2025
Same journal

Behavioral and functional characterization of early-stage Parkinson's disease models reveals attentional deficits and circuit-level connectivity alterations.

Experimental neurology·2026
Same journal

Neuropathological and functional impact of astrocyte-derived extracellular vesicles in an aged model of Alzheimer's disease.

Experimental neurology·2026
Same journal

PI3K/Akt pathway in ischemic stroke: A central regulator of neuronal survival and repair.

Experimental neurology·2026
Same journal

Hepatokines and stellakines in liver and neurological diseases: The liver-brain axis.

Experimental neurology·2026
Same journal

Structural dynamics of α-Synuclein: Multi-scale imaging insights into pathological progression across Synucleinopathies.

Experimental neurology·2026
Same journal

Retraction notice to 'Mitochondrial ferritin upregulation reduced oxidative stress and blood-brain-barrier disruption by maintaining cellular iron homeostasis in a neonatal rat model of germinal matrix hemorrhage' [Experimental Neurology 374 (2024) 114703].

Experimental neurology·2026
See all related articles

Related Experiment Video

Updated: May 4, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

12.4K

Multiple sclerosis: lessons from molecular neuropathology.

Hans Lassmann1

  • 1Center for Brain Research, Medical University of Vienna, Austria.

Experimental Neurology
|December 18, 2013
PubMed
Summary
This summary is machine-generated.

Multiple sclerosis (MS) involves central nervous system inflammation and demyelination. A specific factor in the meninges may trigger cortical lesions, potentially through microglia activation and oxidative stress.

Keywords:
DemyelinationMultiple sclerosisNeurodegeneration

More Related Videos

Two-photon Imaging of Cellular Dynamics in the Mouse Spinal Cord
10:44

Two-photon Imaging of Cellular Dynamics in the Mouse Spinal Cord

Published on: February 22, 2015

9.9K
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

6.5K

Related Experiment Videos

Last Updated: May 4, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

12.4K
Two-photon Imaging of Cellular Dynamics in the Mouse Spinal Cord
10:44

Two-photon Imaging of Cellular Dynamics in the Mouse Spinal Cord

Published on: February 22, 2015

9.9K
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

6.5K

Area of Science:

  • Neuroimmunology
  • Pathology of the Central Nervous System

Background:

  • Multiple sclerosis (MS) is an inflammatory central nervous system disease characterized by demyelination and neuronal injury.
  • The precise mechanisms driving tissue damage in MS remain incompletely understood.
  • Subpial cortical lesions are a unique pathological hallmark exclusively observed in MS patients.

Purpose of the Study:

  • To review the current understanding of MS pathogenesis, focusing on subpial cortical lesions.
  • To explore the potential role of a soluble demyelinating factor originating from meningeal inflammation.
  • To discuss the contribution of oxidative stress and mitochondrial injury to neurodegeneration in MS.

Main Methods:

  • Review of existing literature on MS pathology, focusing on cortical lesions and demyelinating factors.
  • Analysis of proposed mechanisms involving meningeal factors, microglia activation, and oxidative stress.
  • Discussion of the molecular nature and potential targets of demyelinating factors.

Main Results:

  • Confluent subpial cortical lesions are highly specific to MS and suggest a unique pathogenic process.
  • A soluble factor from meningeal inflammation is hypothesized to initiate subpial demyelination.
  • Oxidative stress, driven by microglia, significantly contributes to myelin and neuronal damage, particularly in progressive MS.

Conclusions:

  • The identification of a specific demyelinating factor is crucial for understanding MS pathogenesis.
  • This factor may directly cause demyelination or indirectly through microglia-mediated oxidative injury.
  • Further molecular characterization of this factor could reveal novel therapeutic targets for MS.