Abstract
Experimental autoimmune encephalomyelitis (EAE), a widely recognized animal model of multiple sclerosis (MS), is highly useful for studying inflammation, demyelination, and neurodegeneration in the central nervous system (CNS). EAE exhibits many similarities with MS, which is a chronic inflammatory disease affecting CNS white matter in humans. Various studies have indicated that EAE is a particularly useful animal model for understanding both the mechanisms of immune-mediated CNS pathology and also the progressive clinical course of MS. Demyelination and axonal dysfunction have previously been shown in MS and EAE but current evidences indicate that axonal damage and neuron death also occur, demonstrating that these diseases harbor a neurodegenerative component. Recent studies also have shown that the activation of calpain and caspase pathways contribute to the apoptotic death of oligodendrocytes and neurons, promoting the pathological events leading to neurological deficits. Apoptosis is involved in the disease-regulating as well as in the disease-promoting processes in EAE. This review discusses the major involvement of calpain and caspase pathways in causing demyelination and neurodegeneration in EAE animals.
Keywords: Apoptosis, calpain, caspase, cytokine, demyelination, experimental autoimmune encephalomyelitis, multiple sclerosis, neurodegeneration
CNS & Neurological Disorders - Drug Targets
Title: Activation of Calpain and Caspase Pathways in Demyelination and Neurodegeneration in Animal Model of Multiple Sclerosis
Volume: 7 Issue: 3
Author(s): Arabinda Das, M. Kelly Guyton, Jonathan T. Butler, Swapan K. Ray and Naren L. Banik
Affiliation:
Keywords: Apoptosis, calpain, caspase, cytokine, demyelination, experimental autoimmune encephalomyelitis, multiple sclerosis, neurodegeneration
Abstract: Experimental autoimmune encephalomyelitis (EAE), a widely recognized animal model of multiple sclerosis (MS), is highly useful for studying inflammation, demyelination, and neurodegeneration in the central nervous system (CNS). EAE exhibits many similarities with MS, which is a chronic inflammatory disease affecting CNS white matter in humans. Various studies have indicated that EAE is a particularly useful animal model for understanding both the mechanisms of immune-mediated CNS pathology and also the progressive clinical course of MS. Demyelination and axonal dysfunction have previously been shown in MS and EAE but current evidences indicate that axonal damage and neuron death also occur, demonstrating that these diseases harbor a neurodegenerative component. Recent studies also have shown that the activation of calpain and caspase pathways contribute to the apoptotic death of oligodendrocytes and neurons, promoting the pathological events leading to neurological deficits. Apoptosis is involved in the disease-regulating as well as in the disease-promoting processes in EAE. This review discusses the major involvement of calpain and caspase pathways in causing demyelination and neurodegeneration in EAE animals.
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Cite this article as:
Das Arabinda, Guyton Kelly M., Butler T. Jonathan, Ray K. Swapan and Banik L. Naren, Activation of Calpain and Caspase Pathways in Demyelination and Neurodegeneration in Animal Model of Multiple Sclerosis, CNS & Neurological Disorders - Drug Targets 2008; 7 (3) . https://dx.doi.org/10.2174/187152708784936699
DOI https://dx.doi.org/10.2174/187152708784936699 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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