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

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...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

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...
Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders01:27

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

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 the...

You might also read

Related Articles

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

Sort by
Same author

Lesion network localization of depression in multiple sclerosis.

Nature. Mental health·2026
Same author

A Case of Persistent Ataxia and Atypical Brain Lesions: From the National Multiple Sclerosis Society Case Conference Proceedings.

Neurology(R) neuroimmunology & neuroinflammation·2026
Same author

A cell-intrinsic glucocorticoid biosynthesis and sensing circuit maintains a homeostatic Th17 cell state.

Immunity·2026
Same author

Comorbidities and lifestyle changes as predictors of the multiple sclerosis prodrome: A prospective cohort study.

Multiple sclerosis (Houndmills, Basingstoke, England)·2026
Same author

Cell-type- and state-resolved transcriptomics uncovers distinct T cell and monocyte dysregulation in multiple sclerosis.

Cell reports·2026
Same author

Nasal administration of Protollin enhances monocyte phagocytosis and decreases CD8<sup>+</sup> T cell cytotoxicity in subjects with early Alzheimer's disease: a Phase 1 clinical trial.

npj aging·2026
Same journal

Assessing Sudden Unexpected Death in Epilepsy (SUDEP), Mortality, and Suicide in Pediatric Epilepsy from the lens of Healthcare Disparities: Data From a Scoping Review.

Journal of child neurology·2026
Same journal

The Importance of Accessible, Patient-Focused Language in the Age of the Electronic Medical Record.

Journal of child neurology·2026
Same journal

Genetic Etiologies and Risk Factors for Regressive Autism and Childhood Disintegrative Disorder: A Scoping Review.

Journal of child neurology·2026
Same journal

Birmingham, 1963.

Journal of child neurology·2026
Same journal

Hyperintensity on Diffusion-Weighted Imaging in a MELAS Patient Does Not Necessarily Mean Cytotoxic Edema.

Journal of child neurology·2026
Same journal

Neuromuscular Symptoms of <i>ORAI1</i>-Related Immunodeficiency.

Journal of child neurology·2026
See all related articles

Related Experiment Video

Updated: May 18, 2026

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

Pathogenesis of pediatric multiple sclerosis.

David Vargas-Lowy1, Tanuja Chitnis

  • 1Center for Neurological Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA 02114, USA.

Journal of Child Neurology
|September 7, 2012
PubMed
Summary
This summary is machine-generated.

Pediatric multiple sclerosis (MS) research is advancing, offering insights into disease initiation, biomarkers, and treatment. Understanding childhood MS pathogenesis may reveal general risk factors and differences from adult-onset MS.

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

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

Related Experiment Videos

Last Updated: May 18, 2026

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

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

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

Area of Science:

  • Neurology
  • Immunology
  • Pediatrics

Background:

  • Multiple sclerosis (MS) onset in children affects 3-5% of patients.
  • Knowledge of pediatric MS pathobiology is limited but expanding.

Purpose of the Study:

  • To review current knowledge on pediatric MS pathogenesis.
  • To address key questions regarding disease initiation, biomarkers, pathogenesis differences from adult MS, treatment optimization, and environmental risk factors.

Main Methods:

  • Literature review of pediatric multiple sclerosis.
  • Analysis of current research on pathogenesis and clinical aspects.

Main Results:

  • Discussion of factors influencing pediatric MS initiation and propagation.
  • Exploration of potential biomarkers for disease course.
  • Comparison of pediatric MS pathogenesis with adult-onset MS.
  • Consideration of treatment strategies for pediatric demyelinating diseases.
  • Investigation of insights into general MS environmental risk factors.

Conclusions:

  • Further research into pediatric MS is crucial for understanding MS etiology and improving patient outcomes.
  • Pediatric MS may offer unique insights into the broader spectrum of multiple sclerosis.