A preclinical mice model of multiple sclerosis based on the toxin-induced double-site demyelination of callosal and cerebellar fibers

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dc.article.number48
dc.catalogadorpau
dc.contributor.authorVejar, Sebastián
dc.contributor.authorPizarro, Ignacio S.
dc.contributor.authorPulgar-Sepúlveda, Raúl
dc.contributor.authorVicencio, Sinay C.
dc.contributor.authorPolit, Andrés
dc.contributor.authorAmador, Cristian A.
dc.contributor.authorRio, Rodrigo del
dc.contributor.authorVaras, Rodrigo
dc.contributor.authorOrellana, Juan A.
dc.contributor.authorOrtiz, Fernando C.
dc.date.accessioned2024-08-01T21:12:01Z
dc.date.available2024-08-01T21:12:01Z
dc.date.issued2024
dc.date.updated2024-07-28T00:04:35Z
dc.description.abstractBackground: Multiple sclerosis (MS) is an irreversible progressive CNS pathology characterized by the loss of myelin (i.e. demyelination). The lack of myelin is followed by a progressive neurodegeneration triggering symptoms as diverse as fatigue, motor, locomotor and sensory impairments and/or bladder, cardiac and respiratory dysfunction. Even though there are more than fourteen approved treatments for reducing MS progression, there are still no cure for the disease. Thus, MS research is a very active field and therefore we count with different experimental animal models for studying mechanisms of demyelination and myelin repair, however, we still lack a preclinical MS model assembling demyelination mechanisms with relevant clinical-like signs. Results: Here, by inducing the simultaneous demyelination of both callosal and cerebellar white matter fibers by the double-site injection of lysolecithin (LPC), we were able to reproduce CNS demyelination, astrocyte recruitment and increases levels of proinflammatory cytokines levels along with motor, locomotor and urinary impairment, as well as cardiac and respiratory dysfunction, in the same animal model. Single site LPC-injections either in corpus callosum or cerebellum only, fails in to reproduce such a complete range of MS-like signs. Conclusion: We here report that the double-site LPC injections treatment evoke a complex MS-like mice model. We hope that this experimental approach will help to deepen our knowledge about the mechanisms of demyelinated diseases such as MS.
dc.fechaingreso.objetodigital2024-08-01
dc.format.extent14 páginas
dc.fuente.origenBiomed Central
dc.identifier.citationBiological Research. 2024 Jul 22;57(1):48
dc.identifier.doi10.1186/s40659-024-00529-7
dc.identifier.urihttps://doi.org/10.1186/s40659-024-00529-7
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/87251
dc.identifier.wosidWOS:001273093300001
dc.information.autorucFacultad de Ciencias Biológicas; Rio, Rodrigo del; S/I; 126608
dc.language.isoen
dc.nota.accesocontenido completo
dc.rightsacceso abierto
dc.rights.holderThe Author(s)
dc.subjectMyelin
dc.subjectMultiple sclerosis
dc.subjectWhite matter
dc.subjectNeurodegeneration
dc.subjectNeuroinfammation
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleA preclinical mice model of multiple sclerosis based on the toxin-induced double-site demyelination of callosal and cerebellar fibers
dc.typeartículo
dc.volumen57
sipa.codpersvinculados126608
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