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dc.contributor.authorBernal Chico, Ana
dc.contributor.authorManterola Juaristi, Andrea
dc.contributor.authorMato Santos, Susana ORCID
dc.date.accessioned2020-11-12T18:31:19Z
dc.date.available2020-11-12T18:31:19Z
dc.date.issued2020
dc.identifier.citationEkaia 38 : 241-257 (2020)
dc.identifier.issn0214-9001
dc.identifier.urihttp://hdl.handle.net/10810/47919
dc.description.abstractEsklerosi anizkoitza (EA) nerbio-sistema zentralaren (NSZ) hanturazko gaixotasun desmielinizatzailea da. Gaixotasunaren etiologia zehatza ezagutzen ez den arren, jakina da oligodendrozitoen heriotzarekin eta neuronen endekapenarekin erlazionatutako hantura-lesioak agertzen direla. Gertaera horiek dira, hain zuzen ere, ezgaitasuna eragiten dituztenak pazienteengan. Hala ere, mielinaren birsortze partziala gertatzen da, eta hobekuntza hori bultzatzeko estrategiak dira gaur egun bilatzen direnak. Endokanabinoide-sistemak EAren sintomatologia murrizteko potentziala duela frogatu dute urteetan zehar egindako ikerketek. Zentzu horretan, 2-arakidonoilglizerolaren (2-AG) degradazioa inhibitzeak dirudi estrategia terapeutikorik onena. Monoazilglizerol lipasa (MAGL) entzimak 2-AG-aren proportzio handiena degradatzen du NSZn. Entzima horren inhibizioak, bai desmielinizazioan bai konponketan onurak sustatzen dituen arren, CB1 hartzaileen desentsibilizazioa ere eragiten du. Nahiz eta ABHD familiako hidrolasa 6-k (ABHD6) 2-AG-aren kopuru txikiagoa degradatzen duen egoera basaletan, hantura-egoeretan proportzio handiagoa degradatu egiten du. Horregatik, hanturazko testuinguruetan ABHD6-aren inhibizioa proposatzen da 2-AG mailak igotzeko efektu ez desiragarriak ekiditen diren bitartean. Asmo horrekin, ABHD6-aren inhibitzaile espezifiko baten (KT182) birmielinizazio ahalmena aztertu dugu EA-ren animalia-eredu batean.; Multiple sclerosis (MS) is an inflammatory demyelinating disease of the nervouse central system (CNS). Although the ethiology of the disease remains unknown, of the main hallmarks is the appearance of inflammatory lesions related to the death of oligodendrocytes and neurodegeneration. Those events are, indeed, the cause of disability in the patients. However, there is a partial recovery of the myelin, and nowadays the efforts are focused on finding strategies to enhance this repair. During the last years, numerous researches have shown the potential of the endocannabinoid system to reduce the symptomatology of MS. In this sense, the inhibition of the degradation of 2-arachidonoylglycerol (2-AG) seems the most promising strategy. Monoacylglycerol lipase (MAGL) degrades the majority of the 2-AG in the CNS. Although the blockade of this enzyme protects against demyelination and promotes remyelination, it also induces desensitization of CB1 receptors. Even though in basal conditions alpha/beta-Hydrolase containing domain 6 (ABHD6) hydrolyses a small quantity of 2-AG, it degrades a bigger amount under inflammatory conditions. Thus, ABHD6 inhibition is proposed in inflammatory contexts in order to increase 2-AG levels while avoiding side effects. With this aim, we study the remyelination potential of KT182, a specific ABHD6 inhibitor, in an animal model of MS.
dc.language.isoeus
dc.publisherServicio Editorial de la Universidad del País Vasco/Euskal Herriko Unibertsitatearen Argitalpen Zerbitzua
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/
dc.titleABHD6-aren inhibizioaren azterketa birmielinizazioa bultzatzeko kuprizonaren desmielinizazio primarioaren aniamalia-ereduan
dc.typeinfo:eu-repo/semantics/article
dc.rights.holder© 2020 UPV/EHU Attribution-NonCommercial-ShareAlike 4.0 International
dc.identifier.doi10.1387/ekaia.21355


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© 2020 UPV/EHU Attribution-NonCommercial-ShareAlike 4.0 International
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