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Cannabidiol attenuates cognitive deficits and neuroinflammation induced by early alcohol exposure in a mice model

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dc.contributor.author García Baos, Alba
dc.contributor.author Puig Reyne, Xavier
dc.contributor.author García Algar, Oscar
dc.contributor.author Valverde Granados, Olga
dc.date.accessioned 2021-08-05T05:57:33Z
dc.date.available 2021-08-05T05:57:33Z
dc.date.issued 2021
dc.identifier.citation García-Baos A, Puig-Reyne X, García-Algar Ó, Valverde O. Cannabidiol attenuates cognitive deficits and neuroinflammation induced by early alcohol exposure in a mice model. Biomed Pharmacother. 2021;141:111813. DOI: 10.1016/j.biopha.2021.111813
dc.identifier.issn 0753-3322
dc.identifier.uri http://hdl.handle.net/10230/48314
dc.description.abstract Foetal alcohol spectrum disorder (FASD) is the umbrella term used to describe the physical and mental disabilities induced by alcohol exposure during development. Early alcohol exposure induces cognitive impairments resulting from damage to the central nervous system (CNS). The neuroinflammatory response accompanied by neurodegenerative mechanisms contribute to those detrimental alterations. Cannabidiol (CBD) has recently emerged as an anti-inflammatory drug that might be useful to treat several neuropsychiatric disorders. In our study, we assessed the effects of CBD on long-lasting cognitive deficits induced by early alcohol exposure. Furthermore, we analysed long-term pro-inflammatory and apoptotic markers within the prefrontal cortex and hippocampus. To model alcohol binge drinking during gestational and lactation periods, we used pregnant C57BL/6 female mice with time-limited access to 20% v/v alcohol solution. Following the prenatal and lactation alcohol exposure (PLAE), we treated the male and female offspring with CBD from post-natal day (PD) 25 until PD34, and we evaluated their cognitive performance at PD60. Our results showed that CBD treatment during peri-adolescence period ameliorates cognitive deficits observed in our FASD-like mouse model, without sex differences. Moreover, CBD restores the PLAE-induced increased levels of TNFα and IL-6 in the hippocampus. Thus, our study provides new insights for CBD as a therapeutic agent to counteract cognitive impairments and neuroinflammation caused by early alcohol exposure.
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher Elsevier
dc.relation.ispartof Biomed Pharmacother. 2021;141:111813
dc.rights © 2021 The Author(s). Published by Elsevier Masson SAS. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0).
dc.rights.uri http://creativecommons.org/licenses/by-nc-nd/4.0
dc.title Cannabidiol attenuates cognitive deficits and neuroinflammation induced by early alcohol exposure in a mice model
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.1016/j.biopha.2021.111813
dc.subject.keyword Cannabidiol
dc.subject.keyword Cannabidiol (PubChem CID: 644019)
dc.subject.keyword Cognitive deficits
dc.subject.keyword Ethanol (PubChem CID: 702)
dc.subject.keyword Foetal alcohol spectrum disorder
dc.subject.keyword Neuroinflammation
dc.subject.keyword Prenatal alcohol exposure
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion


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