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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...
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
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mTOR Signaling and Cancer Progression

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Related Experiment Video

Updated: Jul 14, 2026

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

The insulin-like growth factor system in multiple sclerosis.

Daniel Chesik1, Nadine Wilczak, Jacques De Keyser

  • 1Department of Neurology, University Medical Center Groningen, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands.

International Review of Neurobiology
|May 29, 2007
PubMed
Summary

Multiple sclerosis (MS) treatments fail in the progressive phase. Insulin-like growth factor-1 (IGF-1) shows promise for neuroprotection and myelin repair in MS, offering potential restorative therapies.

Related Experiment Videos

Last Updated: Jul 14, 2026

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:

  • Neuroscience
  • Endocrinology
  • Immunology

Background:

  • Multiple sclerosis (MS) is a chronic central nervous system disorder involving inflammation, demyelination, and axonal loss.
  • Current MS therapies are ineffective during the disease's progressive phase, highlighting the need for neuroprotective and restorative treatments.

Purpose of the Study:

  • To explore the role of the Insulin-like Growth Factor (IGF) system in Multiple Sclerosis (MS) pathophysiology.
  • To review preclinical findings on the IGF system in MS models.
  • To discuss the therapeutic potential of IGF-1 for MS.

Main Methods:

  • Literature review of the IGF system's involvement in MS.
  • Analysis of preclinical data from MS models.
  • Discussion of IGF-1's neuroprotective and myelinogenic properties.

Main Results:

  • The IGF system, including IGF-1, IGF-2, and IGF-binding proteins (IGFBPs), plays a role in MS.
  • IGF-1 demonstrates neuroprotective effects and supports oligodendrocyte survival and myelination.
  • Preclinical studies suggest potential benefits of IGF-1 in MS models.

Conclusions:

  • The IGF system is implicated in the pathophysiology of Multiple Sclerosis.
  • IGF-1 exhibits significant neuroprotective and myelinogenic potential, making it a candidate for restorative MS therapies.
  • Further research into IGF-1-based therapies is warranted for progressive MS.