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Title: Memory improvement in the AβPP/PS1 mouse model of familial Alzheimer's disease induced by carbamylated-erythropoietin is accompanied by modulation of synaptic genes
Author: Armand-Ugón, Mercedes
Aso Pérez, Ester
Moreno Castro, Jesús
Riera i Codina, Miquel
Sànchez, Àlex (Sànchez Pla)
Vegas Lozano, Esteban
Ferrer, Isidro (Ferrer Abizanda)
Keywords: Malaltia d'Alzheimer
Receptors de neurotransmissors
Alzheimer's disease
Neurotransmitter receptors
Issue Date: 2015
Publisher: IOS Press
Abstract: Neuroprotection of erythropoietin (EPO) following long-term administration is hampered by the associated undesirable effects on hematopoiesis and body weight. For this reason, we tested carbamylated-EPO (CEPO), which has no effect on erythropoiesis, and compared it with EPO in the AβPP/PS1 mouse model of familial Alzheimer's disease. Groups of 5-month-old wild type (WT) and transgenic mice received chronic treatment consisting of CEPO (2,500 or 5,000 UI/kg) or EPO (2,500 UI/kg) 3 days/week for 4 weeks. Memory at the end of treatment was assessed with the object recognition test. Microarray analysis and quantitative-PCR were used for gene expression studies. No alterations in erythropoiesis were observed in CEPO-treated WT and AβPP/PS1 transgenic mice. EPO and CEPO improved memory in AβPP/PS1 animals. However, only EPO decreased amyloid-β (Aβ) plaque burden and soluble Aβ40. Microarray analysis of gene expression revealed a limited number of common genes modulated by EPO and CEPO. CEPO but not EPO significantly increased gene expression of dopamine receptors 1 and 2, and adenosine receptor 2a, and significantly down-regulated adrenergic receptor α1D and gastrin releasing peptide. CEPO treatment resulted in higher protein levels of dopamine receptors 1 and 2 in WT and AβPP/PS1 animals, whereas the adenosine receptor 2a was reduced in WT animals. The present results suggest that the improved behavior observed in AβPP/PS1 transgenic mice after CEPO treatment may be mediated, at least in part, by the observed modulation of the expression of molecules involved in neurotransmission.
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It is part of: Journal of Alzheimer's Disease, 2015, vol. 45, num. 2, p. 407-421
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ISSN: 1387-2877
Appears in Collections:Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))
Articles publicats en revistes (Genètica, Microbiologia i Estadística)

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