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dc.contributor.authorGarcía-Marchena, Nuria
dc.contributor.authorPizarro, Nieves
dc.contributor.authorPavón, Francisco-Javier
dc.contributor.authorMartínez-Huélamo, Miriam
dc.contributor.authorFlores-López, María
dc.contributor.authorRequena-Ocaña, Nerea
dc.contributor.authorAraos, Pedro
dc.contributor.authorSilva-Peña, Daniel
dc.contributor.authorSuárez, Juan
dc.contributor.authorSantín, Luis J
dc.contributor.authorde la Torre, Rafael
dc.contributor.authorRodríguez de Fonseca, Fernando
dc.contributor.authorSerrano, Antonia
dc.date.accessioned2024-02-12T19:47:36Z
dc.date.available2024-02-12T19:47:36Z
dc.date.issued2020-10-13
dc.identifier.otherhttp://hdl.handle.net/10668/16413
dc.identifier.urihttp://hdl.handle.net/20.500.12105/18134
dc.description.abstractLysophosphatidic acid (LPA) species are bioactive lipids participating in neurodevelopmental processes. The aim was to investigate whether the relevant species of LPA were associated with clinical features of alcohol addiction. A total of 55 abstinent alcohol use disorder (AUD) patients were compared with 34 age/sex/body mass index-matched controls. Concentrations of total LPA and 16:0-LPA, 18:0-LPA, 18:1-LPA, 18:2-LPA and 20:4-LPA species were quantified and correlated with neuroplasticity-associated growth factors including brain derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1) and IGF-2, and neurotrophin-3 (NT-3). AUD patients showed dysexecutive syndrome (22.4%) and memory impairment (32.6%). Total LPA, 16:0-LPA, 18:0-LPA and 18:1-LPA concentrations, were decreased in the AUD group compared to control group. Total LPA, 16:0-LPA, 18:2-LPA and 20:4-LPA concentrations were decreased in men compared to women. Frontal lobe functions correlated with plasma LPA species. Alcohol-cognitive impairments could be related with the deregulation of the LPA species, especially in 16:0-LPA, 18:1-LPA and 20:4-LPA. Concentrations of BDNF correlated with total LPA, 18:2-LPA and 20:4-LPA species. The relation between LPA species and BDNF is interesting in plasticity and neurogenesis functions, their involvement in AUD might serve as a biomarker of cognitive impairment.
dc.language.isoeng
dc.type.hasVersionVoR
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subject.meshAdolescent 
dc.subject.meshAdult 
dc.subject.meshAged 
dc.subject.meshAlcoholism 
dc.subject.meshBiomarkers 
dc.subject.meshBrain-Derived Neurotrophic Factor 
dc.subject.meshCognitive Dysfunction 
dc.subject.meshEthanol 
dc.subject.meshFemale 
dc.subject.meshHumans 
dc.subject.meshInsulin-Like Growth Factor I 
dc.subject.meshInsulin-Like Growth Factor II 
dc.subject.meshLysophospholipids 
dc.subject.meshMale 
dc.subject.meshMiddle Aged 
dc.subject.meshNeurotrophin 3 
dc.subject.meshOutpatients 
dc.subject.meshPlasma 
dc.subject.meshYoung Adult 
dc.titlePotential association of plasma lysophosphatidic acid (LPA) species with cognitive impairment in abstinent alcohol use disorders outpatients.
dc.typeresearch article
dc.rights.licenseAttribution 4.0 International*
dc.identifier.pubmedID33051508es_ES
dc.format.volume10es_ES
dc.format.number1es_ES
dc.format.page17163es_ES
dc.identifier.doi10.1038/s41598-020-74155-0
dc.identifier.e-issn2045-2322es_ES
dc.identifier.journalScientific reportses_ES
dc.rights.accessRightsopen accesses_ES


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Attribution 4.0 International
Este Item está sujeto a una licencia Creative Commons: Attribution 4.0 International