| Literature DB >> 25431839 |
Genaro Gabriel Ortiz1, Fermín Paul Pacheco-Moisés2, Miguel Ángel Macías-Islas3, Luis Javier Flores-Alvarado4, Mario A Mireles-Ramírez3, Erika Daniela González-Renovato5, Vanessa Elizabeth Hernández-Navarro5, Angélica Lizeth Sánchez-López5, Moisés Alejandro Alatorre-Jiménez5.
Abstract
Multiple sclerosis (MS) is an autoimmune disease of the central nervous system associated with demyelination and axonal loss eventually leading to neurodegeneration. MS exhibits many of the hallmarks of an inflammatory autoimmune disorder including breakdown of the blood-brain barrier (BBB). The BBB is a complex organization of cerebral endothelial cells, pericytes and their basal lamina, which are surrounded and supported by astrocytes and perivascular macrophages. In pathological conditions, lymphocytes activated in the periphery infiltrate the central nervous system to trigger a local immune response that ultimately damages myelin and axons. Cytotoxic factors including pro-inflammatory cytokines, proteases, and reactive oxygen and nitrogen species accumulate and may contribute to myelin destruction. Dysregulation of the BBB and transendothelial migration of activated leukocytes are among the earliest cerebrovascular abnormalities seen in MS brains and parallel the release of inflammatory cytokines. In this review we establish the importance of the role of the BBB in MS. Improvements in our understanding of molecular mechanism of BBB functioning in physiological and pathological conditions could lead to improvement in the quality of life of MS patients.Entities:
Keywords: Blood–brain barrier; Central nervous system; Multiple sclerosis; Oxidative stress
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Year: 2014 PMID: 25431839 DOI: 10.1016/j.arcmed.2014.11.013
Source DB: PubMed Journal: Arch Med Res ISSN: 0188-4409 Impact factor: 2.235