Early synaptic deficits in the APP/PS1 mouse model of Alzheimer’s disease involve neuronal adenosine A2A receptors

Hippocampal synaptic dysfunctions are an early symptom of Alzheimer’s disease. Here, the authors find adenosine A2A receptors are up-regulated in APP/PS1 model mice and that deleting or blocking receptor activity helps alleviate plasticity and memory impairments.

Guardado en:
Detalles Bibliográficos
Autores principales: Silvia Viana da Silva, Matthias Georg Haberl, Pei Zhang, Philipp Bethge, Cristina Lemos, Nélio Gonçalves, Adam Gorlewicz, Meryl Malezieux, Francisco Q. Gonçalves, Noëlle Grosjean, Christophe Blanchet, Andreas Frick, U Valentin Nägerl, Rodrigo A. Cunha, Christophe Mulle
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2016
Materias:
Q
Acceso en línea:https://doaj.org/article/1ea75979789f4071b6f94deca86c19df
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:1ea75979789f4071b6f94deca86c19df
record_format dspace
spelling oai:doaj.org-article:1ea75979789f4071b6f94deca86c19df2021-12-02T16:58:00ZEarly synaptic deficits in the APP/PS1 mouse model of Alzheimer’s disease involve neuronal adenosine A2A receptors10.1038/ncomms119152041-1723https://doaj.org/article/1ea75979789f4071b6f94deca86c19df2016-06-01T00:00:00Zhttps://doi.org/10.1038/ncomms11915https://doaj.org/toc/2041-1723Hippocampal synaptic dysfunctions are an early symptom of Alzheimer’s disease. Here, the authors find adenosine A2A receptors are up-regulated in APP/PS1 model mice and that deleting or blocking receptor activity helps alleviate plasticity and memory impairments.Silvia Viana da SilvaMatthias Georg HaberlPei ZhangPhilipp BethgeCristina LemosNélio GonçalvesAdam GorlewiczMeryl MalezieuxFrancisco Q. GonçalvesNoëlle GrosjeanChristophe BlanchetAndreas FrickU Valentin NägerlRodrigo A. CunhaChristophe MulleNature PortfolioarticleScienceQENNature Communications, Vol 7, Iss 1, Pp 1-11 (2016)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Silvia Viana da Silva
Matthias Georg Haberl
Pei Zhang
Philipp Bethge
Cristina Lemos
Nélio Gonçalves
Adam Gorlewicz
Meryl Malezieux
Francisco Q. Gonçalves
Noëlle Grosjean
Christophe Blanchet
Andreas Frick
U Valentin Nägerl
Rodrigo A. Cunha
Christophe Mulle
Early synaptic deficits in the APP/PS1 mouse model of Alzheimer’s disease involve neuronal adenosine A2A receptors
description Hippocampal synaptic dysfunctions are an early symptom of Alzheimer’s disease. Here, the authors find adenosine A2A receptors are up-regulated in APP/PS1 model mice and that deleting or blocking receptor activity helps alleviate plasticity and memory impairments.
format article
author Silvia Viana da Silva
Matthias Georg Haberl
Pei Zhang
Philipp Bethge
Cristina Lemos
Nélio Gonçalves
Adam Gorlewicz
Meryl Malezieux
Francisco Q. Gonçalves
Noëlle Grosjean
Christophe Blanchet
Andreas Frick
U Valentin Nägerl
Rodrigo A. Cunha
Christophe Mulle
author_facet Silvia Viana da Silva
Matthias Georg Haberl
Pei Zhang
Philipp Bethge
Cristina Lemos
Nélio Gonçalves
Adam Gorlewicz
Meryl Malezieux
Francisco Q. Gonçalves
Noëlle Grosjean
Christophe Blanchet
Andreas Frick
U Valentin Nägerl
Rodrigo A. Cunha
Christophe Mulle
author_sort Silvia Viana da Silva
title Early synaptic deficits in the APP/PS1 mouse model of Alzheimer’s disease involve neuronal adenosine A2A receptors
title_short Early synaptic deficits in the APP/PS1 mouse model of Alzheimer’s disease involve neuronal adenosine A2A receptors
title_full Early synaptic deficits in the APP/PS1 mouse model of Alzheimer’s disease involve neuronal adenosine A2A receptors
title_fullStr Early synaptic deficits in the APP/PS1 mouse model of Alzheimer’s disease involve neuronal adenosine A2A receptors
title_full_unstemmed Early synaptic deficits in the APP/PS1 mouse model of Alzheimer’s disease involve neuronal adenosine A2A receptors
title_sort early synaptic deficits in the app/ps1 mouse model of alzheimer’s disease involve neuronal adenosine a2a receptors
publisher Nature Portfolio
publishDate 2016
url https://doaj.org/article/1ea75979789f4071b6f94deca86c19df
work_keys_str_mv AT silviavianadasilva earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT matthiasgeorghaberl earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT peizhang earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT philippbethge earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT cristinalemos earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT neliogoncalves earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT adamgorlewicz earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT merylmalezieux earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT franciscoqgoncalves earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT noellegrosjean earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT christopheblanchet earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT andreasfrick earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT uvalentinnagerl earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT rodrigoacunha earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
AT christophemulle earlysynapticdeficitsintheappps1mousemodelofalzheimersdiseaseinvolveneuronaladenosinea2areceptors
_version_ 1718382374449840128