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

Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
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...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which leads...
Atherosclerosis III: Management01:26

Atherosclerosis III: Management

Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
Autoimmune Disorders01:29

Autoimmune Disorders

Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune system...

You might also read

Related Articles

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

Sort by
Same author

Does Job Role Matter? Food Safety Knowledge and Training Effectiveness Among Food Handlers in Collective Catering.

Foods (Basel, Switzerland)·2026
Same author

IL-1 polymorphisms modulates functional recovery following rehabilitation in multiple sclerosis.

Frontiers in immunology·2026
Same author

Profiling the long-term risk of severe adverse events in a cohort of multiple sclerosis patients treated with different treatment sequences: Results from the Italian Multiple Sclerosis and Related Disorders Registry (I-MS&RD) (ProSA study).

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

Beyond GLM: Inter-Subject Variability as a Complementary Approach to Detect Longitudinal Changes in Emotion Processing in Multiple Sclerosis.

Journal of imaging·2026
Same author

Amyloid-beta-targeting monoclonal antibodies for people with mild cognitive impairment or mild dementia due to Alzheimer's disease.

The Cochrane database of systematic reviews·2026
Same author

Serum miR-199a-3p and miR-103a-3p are possible biomarkers for the onset of multiple sclerosis.

Scientific reports·2026

Related Experiment Video

Updated: May 18, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
10:00

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

Published on: March 24, 2015

Interferon β for secondary progressive multiple sclerosis: a systematic review.

Loredana La Mantia1, Laura Vacchi, Marco Rovaris

  • 1Multiple Sclerosis Centre, Neurorehabilitation Unit, IRCCS Santa Maria Nascente Fondazione Don Gnocchi, Via Capecelatro 66, I-20148 Milano, Italy. lamantialore@gmail.com

Journal of Neurology, Neurosurgery, and Psychiatry
|September 7, 2012
PubMed
Summary

Recombinant beta interferons (IFNβ) do not slow disability progression in secondary progressive multiple sclerosis (SPMS) over three years. While IFNβ reduced relapse risk, it did not prevent established disease progression.

More Related Videos

Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis
06:19

Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis

Published on: September 9, 2022

Related Experiment Videos

Last Updated: May 18, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
10:00

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

Published on: March 24, 2015

Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis
06:19

Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis

Published on: September 9, 2022

Area of Science:

  • Neurology
  • Immunology
  • Clinical Trials

Background:

  • The efficacy of recombinant beta interferons (IFNβ) in secondary progressive multiple sclerosis (SPMS) remains uncertain.
  • Investigating the potential of IFNβ to mitigate disability and cognitive decline in SPMS is crucial.

Purpose of the Study:

  • To evaluate the effectiveness of IFNβ in reducing disability progression in SPMS patients.
  • To assess the impact of IFNβ on cognitive impairment progression in SPMS.

Main Methods:

  • A systematic review and meta-analysis adhering to Cochrane methodology was conducted.
  • Included randomized placebo-controlled trials of IFNβ in SPMS patients from 1995 to March 2012.
  • Data from 5 trials involving 3082 patients were analyzed.

Main Results:

  • After three years, IFNβ did not significantly reduce disability progression (RR 0.98, 95% CI 0.82 to 1.16).
  • A statistically significant, though small, reduction in relapse risk was observed during the first three years (RR 0.91, 0.84 to 0.97).
  • Cognitive data analysis was not feasible; however, adverse events led to more dropouts in the IFNβ group compared to placebo.

Conclusions:

  • Three-year treatment with IFNβ does not delay permanent disability progression in SPMS.
  • IFNβ treatment demonstrates an anti-inflammatory effect by reducing relapse risk.
  • The findings suggest that IFNβ's anti-inflammatory capacity is insufficient to halt MS progression once established.