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Título del libro: Adenosine: A Key Link Between Metabolism And Brain Activity
Título del capítulo: Adenosine and multiple sclerosis

Autores UNAM:
ROGELIO ARELLANO OSTOA;
Autores externos:

Idioma:
Inglés
Año de publicación:
2013
Palabras clave:

Demyelination; EAE; Myelin; Neuroinflammation; Oligodendrocyte; P1 purinergic receptor; Tissue damage


Resumen:

The major demyelinating disease of the CNS is multiple sclerosis (MS), which is the foremost disabling pathology among young adults. MS is a chronic, degenerative disease characterized by focal lesions with inflammation, demyelination, infiltration of immune cells, oligodendroglial death, and axonal degeneration. These cellular alterations are accompanied by neurological deficits, such as sensory disturbances, lack of motor coordination, and visual impairment. It is widely accepted that the etiology of this illness has autoimmune and inflammatory grounds, and that a derailment of the immune system leads to cell- and antibody-mediated attacks on myelin. Both genetic and environmental factors contribute to MS susceptibility. Among them, primary and/or secondary alterations in neurotransmitter signaling including the glutamate and purinergic system lead to oligodendrocyte and myelin damage and contribute to MS pathology. In addition, recent data indicate that adenosine is involved in neuroinflammation, and that activation of adenosine receptors may contribute to tissue damage in experimental models of MS. Moreover, some alterations of adenosine metabolism occur in MS though it is not clear yet whether they are primary or secondary to the disease process. Finally, emerging evidence suggests that enhanced activity of the adenosinergic system may also contribute to the pathophysiology of MS and that this feature may open new therapeutic approaches beneficial for the treatment of MS. © 2013 Springer Science+Business Media New York. All rights are reserved.


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