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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 Eritropoetina Alzheimer's disease Neurotransmitter receptors Erythropoietin |
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. |
Note: | Reproducció del document publicat a: http://dx.doi.org/10.3233/JAD-141389 |
It is part of: | Journal of Alzheimer's Disease, 2015, vol. 45, num. 2, p. 407-421 |
URI: | http://hdl.handle.net/2445/67988 |
Related resource: | http://dx.doi.org/10.3233/JAD-141389 |
ISSN: | 1387-2877 |
Appears in Collections: | Articles publicats en revistes (Genètica, Microbiologia i Estadística) Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
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