Potential association of plasma lysophosphatidic acid (LPA) species with cognitive impairment in abstinent alcohol use disorders outpatients

García Marchena, Nuria; Pizarro Lozano, Mª Nieves; Pavón, Francisco Javier; Martínez-Huélamo, Miriam; Flores López, María; Requena-Ocaña, Nerea; Araos, Pedro; Silva Peña, Daniel; Suárez, Juan; Santín, Luis Javier; Torre Fornell, Rafael de la; Rodríguez de Fonseca, Fernando; Serrano, Antonia

doi:http://dx.doi.org/10.1038/s41598-020-74155-0

Potential association of plasma lysophosphatidic acid (LPA) species with cognitive impairment in abstinent alcohol use disorders outpatients

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García-Marchena N, Pizarro N, Pavón FJ, Martínez-Huélamo M, Flores-López M, Requena-Ocaña N, Araos P, Silva-Peña D, Suárez J, Santín LJ, de la Torre R, Rodríguez de Fonseca F, Serrano A. Potential association of plasma lysophosphatidic acid (LPA) species with cognitive impairment in abstinent alcohol use disorders outpatients. Sci Rep. 2020; 10(1):17163. DOI: 10.1038/s41598-020-74155-0

Abstract

Lysophosphatidic 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.