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http://hdl.handle.net/2445/96453
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DC Field | Value | Language |
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dc.contributor.author | Aso Pérez, Ester | - |
dc.contributor.author | Palomer, Ernest | - |
dc.contributor.author | Juvés, Salvador | - |
dc.contributor.author | Maldonado, Rafael, 1961- | - |
dc.contributor.author | Muñoz, Francisco J. | - |
dc.contributor.author | Ferrer, Isidro (Ferrer Abizanda) | - |
dc.date.accessioned | 2016-03-14T13:53:18Z | - |
dc.date.available | 2016-03-14T13:53:18Z | - |
dc.date.issued | 2012 | - |
dc.identifier.issn | 1387-2877 | - |
dc.identifier.uri | http://hdl.handle.net/2445/96453 | - |
dc.description.abstract | The present study shows that chronic administration of the Cannabinoid receptor type 1 (CB1) receptor agonist arachidonyl-2-chloroethylamide (ACEA) at pre-symptomatic or at early symptomatic stages, at a non-amnesic dose, reduces the cognitive impairment observed in double AβPP(swe)/PS1(1dE9) transgenic mice from 6 months of age onwards. ACEA has no effect on amyloid-β (Aβ) production, aggregation, or clearance. However, ACEA reduces the cytotoxic effect of Aβ42 oligomers in primary cultures of cortical neurons, and reverses Aβ-induced dephosphorylation of glycogen synthase kinase-3β (GSK3β) in vitro and in vivo. Reduced activity of GSK3β in ACEA-treated mice is further supported by the reduced amount of phospho-tau (Thr181) in neuritic processes around Aβ plaques. In addition, ACEA-treated mice show decreased astroglial response in the vicinity of Aβ plaques and decreased expression of the pro-inflammatory cytokine interferon-γ in astrocytes when compared with age-matched vehicle-treated transgenic mice. Our present results show a beneficial effect of ACEA at both the neuronal, mediated at least in part by GSK3β inhibition, and glial levels, resulting in a reduction of reactive astrocytes and lower expression of interferon-γ. As a consequence, targeting the CB1 receptor could offer a versatile approach for the treatment of Alzheimer's disease. | - |
dc.format.extent | 21 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | IOS Press | - |
dc.relation.isformatof | Reproducció del document publicat a: http://dx.doi.org/10.3233/JAD-2012-111862 | - |
dc.relation.ispartof | Journal of Alzheimer's Disease, 2012, vol. 30, num. 2, p. 439-459 | - |
dc.relation.uri | http://dx.doi.org/10.3233/JAD-2012-111862 | - |
dc.rights | (c) Asó, Ester et al., 2012 | - |
dc.source | Articles publicats en revistes (Patologia i Terapèutica Experimental) | - |
dc.subject.classification | Malaltia d'Alzheimer | - |
dc.subject.classification | Cànnabis | - |
dc.subject.classification | Cognició | - |
dc.subject.classification | Neurones | - |
dc.subject.other | Alzheimer's disease | - |
dc.subject.other | Cannabis | - |
dc.subject.other | Cognition | - |
dc.subject.other | Neurons | - |
dc.title | CB1 agonist ACEA protects neurons and reduces the cognitive impairment of AβPP/PS1 mice | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.identifier.idgrec | 631816 | - |
dc.date.updated | 2016-03-14T13:53:23Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 22451318 | - |
Appears in Collections: | Articles publicats en revistes (Patologia i Terapèutica Experimental) Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
Files in This Item:
File | Description | Size | Format | |
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631816.pdf | 1.61 MB | Adobe PDF | View/Open |
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