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Oligodendrocytes, Myelin, & Lesions
In Multiple Sclerosis

  1. Oligodendrocytes have a key role in the development of CNS function and in Myelin related diseases
    Lakartidningen 2000 Jul 12;97(28-29):3265-8

  2. Multiple Sclerosis associated with Peripheral DeMyelinating Neuropathy
    Clin Neuropathol 1996 May-Jun;15(3):135-8

  3. Experimental strategies to promote Central Nervous System ReMyelination in Multiple Sclerosis: insights gained from the Theiler's virus model system
    J NeuroSci Res 1995 Jun 15;41(3):291-6

  4. Multiple Sclerosis: role of growth factors and ReMyelination
    Presse Med 1994 Nov 5;23(34):1577-81

  5. Oligodendrocyte injury is an early event in lesions of Multiple Sclerosis
    Mayo Clin Proc 1993 Jul;68(7):627-36

  6. The distribution of Myelin-associated GlycoProtein and Myelin Basic Protein in actively DeMyelinating Multiple Sclerosis lesions
    J NeuroImmunol 1984 Jul;6(4):251-64




#1

Oligodendrocytes Have A Key Role In The Development Of CNS Function And In Myelin Related Diseases

Anderson ES, Bjartmar C
Lakartidningen 2000 Jul 12;97(28-29):3265-8
Institutionen for biomedicin och kirurgi, Halso-universitetet, Linkoping
PMID# 10997013; UI# 20451566
Abstract

Oligodendrocytes provide CNS Axons with Myelin Sheaths through processes of various lengths.

The lipid-rich Myelin insulates Axons electrically, which increases Conduction velocity. In addition, Oligodendrocytes have Trophic effects on Axons.

During development immature Oligodendrocytes undergo controlled migration, proliferation and differentiation, influenced by various Growth Factors and Axons.

A number of Genetically manipulated animal models have provided insights regarding Myelination and the function of Myelin components.

Current research on Myelin related diseases, i.e. Multiple Sclerosis, focus on novel strategies for ReMyelination through transplantation of Myelinating Cells or stimulation of endogenous Oligodendrocytes.



#2

Multiple Sclerosis Associated With
Peripheral DeMyelinating Neuropathy

Di Trapani G, Carnevale A, Cioffi RP, Massaro AR, Profice P
Clin Neuropathol 1996 May-Jun;15(3):135-8
Catholic University, Institute of Neurology, Policlinico A. Gemelli, Rome, Italy
PMID# 8793246; UI# 96385388
Abstract

We report clinical, ElectroPhysiological, Magnetic Resonance Imaging, and Nerve Biopsy findings of 2 patients with definite Multiple Sclerosis and Peripheral DeMyelinating Disease.

Although it is not easy to assess the real incidence of Peripheral Neuropathy in patients with Multiple Sclerosis, this association seems to be rare.

The combination of Central and Peripheral DeMyelination may be a fortuitous coincidence, but it appears improbable.

Alternatively, these patients may represent a specific subpopulation and common ImmunoPathoGenetic mechanisms such as (Immunological factors, Endothelial alterations, and abnormal expression of Adhesion Molecules) may underly both Central and Peripheral Myelin involvement.

The study of these cases might clarify specific mechanisms of PathoGenetic significance in DeMyelinating Diseases.



#3

Experimental Strategies To Promote CNS ReMyelination In Multiple Sclerosis

Insights gained from the Theiler's virus model system.

Miller DJ, Asakura K, Rodriguez M
J NeuroSci Res 1995 Jun 15;41(3):291-6
Mayo Clinic and Foundation, Dept of Immunology, Rochester, Minnesota 55905, US
PMID# 7563222; UI# 96028306
Abstract

The destruction of Central Nervous System (CNS) Myelin, the lipid-rich insulator surrounding Axons in the mammalian Brain and Spinal Cord, is the primary pathological finding in Multiple Sclerosis.

Myelin loss can result in a significant clinical deficit, and was originally thought to be permanent, similar to Axonal destruction.

However, Myelin regeneration is now an established phenomenon in both human disease and animal models of CNS DeMyelination.

In this review, the concept of ReMyelination in DeMyelinating Diseases such as Multiple Sclerosis is discussed.

And the usefulness of animal models of CNS DeMyelination in developing experimental strategies to promote ReMyelination is examined.

Special emphasis is given to the Theiler's Murine EncephaloMyelitis model, which has been the primary animal model used to investigate therapies designed specifically to stimulate Myelin repair.



#4

Multiple Sclerosis: Role Of Growth Factors And ReMyelination

Lubetzki C
Presse Med 1994 Nov 5;23(34):1577-81
Hopital de la Salpetriere, INSERM U-134, Paris, France
PMID# 7824494; UI# 95124957
Abstract

Multiple Sclerosis is a frequent and often disabling Neurological Disease. Its Etiology and treatment remain to be discovered.

It has been demonstrated in Multiple Sclerosis Brains that ReMyelination can occur after the Myelin damage.

This Myelin repair is achieved by Oligodendrocytes, which are the Myelinating Cells of the Central Nervous System or by Oligodendrocytes precursors still present in adult Central Nervous System.

Several recently discovered Growth Factors can stimulate Oligodendrocytes precursors migration and proliferation, or act as survival factors for mature Oligodendrocytes.

These Glial Growth Factors may represent a new therapeutic approach in Multiple Sclerosis, aiming at the stimulation of the endogenous capacities of ReMyelination.



#5

Oligodendrocyte Injury Is An Early Event In Lesions Of Multiple Sclerosis

Rodriguez M, Scheithauer BW, Forbes G, Kelly PJ
Mayo Clin Proc 1993 Jul;68(7):627-36
Mayo Clinic, Dept of Neurology, Rochester, MN 55905
PMID# 8350635; UI# 93353920
Abstract

The ultrastructural features of 11 stereotaxic Brain biopsy specimens that demonstrated inflammatory primary DeMyelination consistent with acute Multiple Sclerosis were examined.

Uniform widening of inner Myelin lamellae (Biphasic Myelinopathy) and degeneration of inner Glial loops ("dying-back" OligodendroGliopathy) were early pathologic abnormalities.

That antedated complete destruction of Myelin Sheaths.

PeriVascular Inflammatory Cells (Lymphocytes , Macrophages, and occasional Plasma Cells) were in intimate contact with degenerating Myelin sheaths.

The response of Astrocytes was prominent, even in areas of minimal DeMyelination.

Oligodendrocytes were morphologically preserved in early lesions but proliferated at the periphery of active lesions.

Thinly Myelinated Axons indicative of Central Nervous System-type ReMyelination by Oligodendrocytes were observed primarily at the edge of plaques.

Disturbances of the Myelinating function of Oligodendrocytes - unaccompanied by death of these cells - may be among the earliest pathologic features in Multiple Sclerosis.

  • Comment in: Mayo Clin Proc 1993 Jul;68(7):711-2


#6

The Distribution Of Myelin-Associated GlycoProtein And Myelin Basic Protein In Actively DeMyelinating MS Lesions

Prineas JW, Kwon EE, Sternberger NH, Lennon VA
J NeuroImmunol 1984 Jul;6(4):251-64
PMID# 6203933; UI# 84240247
Abstract

Active plaques from 4 patients with Multiple Sclerosis were examined for Myelin-Associated Glycoprotein (MAG) and Myelin Basic Protein (MBP).

Using the Peroxidase-AntiPeroxidase (PAP) ImmunoCytoChemical procedure applied to paraffin sections.

MBP loss was intimately related to the presence of infiltrating Macrophages which appeared to remove MBP-positive fragments directly off intact Myelin sheaths. Phagocytosis of MAG-positive Myelin sheaths was also observed.

These findings support previous morphological studies that suggest that Phagocytosis by Macrophages of Myelin attached to Axons is an important mechanism of DeMyelination in Multiple Sclerosis.



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