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

Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids01:21

Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids

Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2 (COX-2),...
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel Disease...
Inflammatory Bowel Disease IV: Pharmacological Management01:29

Inflammatory Bowel Disease IV: Pharmacological Management

Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...
Antiasthma Drugs: Inhaled Corticosteroids and Glucocorticoids01:25

Antiasthma Drugs: Inhaled Corticosteroids and Glucocorticoids

Inhaled corticosteroids (ICS) are anti-inflammatory drugs used primarily in treating persistent asthma and providing long-term maintenance. They target the bronchial mucosa, the lining of the airways, to control inflammation, a critical factor in asthma progression and exacerbation.
ICS work through a multifaceted mechanism of action. They suppress the inflammatory response caused by the proliferation of TH cells. They also reduce the transcription of the IL-2 gene, which is involved in the...
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...
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...

You might also read

Related Articles

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

Sort by
Same author

Recent Progress on Selenium Nanoparticles: Synthesis and Neuroprotective Effects for the Treatment of Alzheimer's Disease.

Molecular neurobiology·2026
Same author

DNA methylation signatures from peripheral blood revealed epigenetic alterations in Fanconi anemia.

Human genetics·2026
Same author

Communication when bone and joint infection in children is suspected : a qualitative study of patients, families, and health professionals.

Bone & joint open·2026
Same author

Decanoic Acid Treatment Alleviates Non-cell Autonomous Transfer of HD Pathology by Secretome of Mutant Huntingtin Expressing Cells.

Neurochemical research·2026
Same author

A Rare Variant in RPS26 Gene Causing Variable Phenotype of Diamond-Blackfan Anemia Type 10 (DBA10) in an Indian Family.

Indian journal of pediatrics·2025
Same author

Real-World Data on the Practice of Chemoradiation with Select Cohort Consolidation Chemotherapy in High-Risk Locally Advanced Rectal Cancers (SOLAR study).

South Asian journal of cancer·2025

Related Experiment Video

Updated: Jul 11, 2026

Determining Immune System Suppression versus CNS Protection for Pharmacological Interventions in Autoimmune Demyelination
09:38

Determining Immune System Suppression versus CNS Protection for Pharmacological Interventions in Autoimmune Demyelination

Published on: September 12, 2016

Corticosteroids for multiple sclerosis: II. Application for disease-modifying effects.

Anjali Shah1, Eric Eggenberger, Robert Zivadinov

  • 1Department of Neurology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75235, USA. elliot.frohman@utsouthwestern.edu

Neurotherapeutics : the Journal of the American Society for Experimental Neurotherapeutics
|October 9, 2007
PubMed
Summary
This summary is machine-generated.

Managing multiple sclerosis (MS) requires addressing ongoing disease activity despite disease-modifying agents (DMAs). This review explores intensifying treatment, including corticosteroids (CS), for persistent MS progression.

Related Experiment Videos

Last Updated: Jul 11, 2026

Determining Immune System Suppression versus CNS Protection for Pharmacological Interventions in Autoimmune Demyelination
09:38

Determining Immune System Suppression versus CNS Protection for Pharmacological Interventions in Autoimmune Demyelination

Published on: September 12, 2016

Area of Science:

  • Neurology
  • Immunology

Background:

  • Patients with multiple sclerosis (MS) often show persistent disease activity (exacerbations, functional decline, cognitive impairment, radiologic progression) even while on disease-modifying agents (DMAs).
  • Factors like nonadherence or neutralizing antibodies may contribute, but often partial treatment effects necessitate further management strategies.

Purpose of the Study:

  • To review the rationale and practical approaches for intensifying treatment in multiple sclerosis (MS).
  • To focus on the use of corticosteroids (CS) and adrenocorticotropic hormone (ACTH) for modifying ongoing disease activity in MS.

Main Methods:

  • Review of existing literature on treatment intensification for multiple sclerosis (MS).
  • Discussion of combination therapy strategies, including the use of corticosteroids (CS) and ACTH.

Main Results:

  • Limited evidence supports the routine use of CS and ACTH for chronic disease modification in progressive MS.
  • Factors influencing combination treatment plans for MS are complex.

Conclusions:

  • Intensifying treatment for MS requires careful consideration of various factors when patients show inadequate response to initial DMAs.
  • Further research is needed to establish evidence-based regimens for using CS and ACTH in chronic MS management.