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

Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

2.5K
Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
2.5K
Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders01:27

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

2.5K
Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within...
2.5K

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

Spatial protein profiling reveals active roles for astrocytes in the chronic active lesion core during multiple sclerosis.

Acta neuropathologica·2025
Same journal

Resolution of expression of concern-Serotonergic pathology and disease burden in the premotor and motor phase of A53T α-synuclein parkinsonism: a cross-sectional study.

The Lancet. Neurology·2026
Same journal

UCL Queen Square Institute of Neurology: 75 years of innovation.

The Lancet. Neurology·2026
Same journal

Correction to Lancet Neurol 2026; 25: 631.

The Lancet. Neurology·2026
Same journal

Epstein-Barr virus and multiple sclerosis: from associations to mechanisms to potential therapies.

The Lancet. Neurology·2026
Same journal

Correction to Lancet Neurol 2025; 24: 740-52.

The Lancet. Neurology·2026
Same journal

Correction to Lancet Neurol 2026; 25: 357-67.

The Lancet. Neurology·2026
See all related articles

Related Experiment Video

Updated: Apr 16, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

12.2K

Pathological mechanisms in progressive multiple sclerosis.

Don H Mahad1, Bruce D Trapp2, Hans Lassmann3

  • 1Centre for Neuroregeneration, University of Edinburgh, Edinburgh, UK.

The Lancet. Neurology
|March 17, 2015
PubMed
Summary
This summary is machine-generated.

Neurodegeneration in multiple sclerosis (MS) is driven by inflammation, brain aging, and accumulated damage. Effective treatments for progressive MS require anti-inflammatory, regenerative, and neuroprotective approaches.

More Related Videos

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

5.4K
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: Apr 16, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

12.2K
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

5.4K
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) is a chronic inflammatory demyelinating disease.
  • Neurodegeneration significantly contributes to disability progression in MS.
  • Current understanding of neurodegenerative mechanisms in progressive MS is incomplete.

Purpose of the Study:

  • To elucidate the pathological mechanisms driving neurodegeneration in multiple sclerosis.
  • To identify key factors contributing to neurodegeneration in progressive MS.
  • To inform the development of effective therapeutic strategies for progressive MS.

Main Methods:

  • Review and synthesis of existing evidence on MS pathology.
  • Analysis of proposed mechanisms linking inflammation, aging, and neurodegeneration.
  • Identification of critical cellular and molecular pathways involved.

Main Results:

  • Early MS inflammation triggers neurodegenerative cascades amplified by brain aging and disease burden.
  • Key drivers include microglia activation, oxidative injury, axonal mitochondrial damage, and iron accumulation.
  • Altered axonal mitochondrial function is a critical factor leading to cell death.

Conclusions:

  • Neurodegeneration in MS is a multifactorial process involving inflammation, aging, and cellular damage.
  • Targeting microglia, oxidative stress, mitochondria, and iron may offer therapeutic benefits.
  • Combined anti-inflammatory, regenerative, and neuroprotective strategies are recommended for progressive MS treatment.