nAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse

Abstract An evaluation of the APPswe/PS1dE9 transgenic AD mouse, presenting with the toxic Aβ1-42 deposition found in human AD, allowed us to characterize time-dependent changes in inflammatory and cholinergic markers present in AD. Astrogliosis was observed in cortex and hippocampus, with cellular...

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Autores principales:	D’Angelo Chiara, Costantini Erica, Salvador Nieves, Marchioni Michele, Di Nicola Marta, Greig H. Nigel, Reale Marcella
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c4aad8a0c7404052a401dc4f37a93ef6
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spelling	oai:doaj.org-article:c4aad8a0c7404052a401dc4f37a93ef62021-12-02T14:49:34ZnAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse10.1038/s41598-021-89139-x2045-2322https://doaj.org/article/c4aad8a0c7404052a401dc4f37a93ef62021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-89139-xhttps://doaj.org/toc/2045-2322Abstract An evaluation of the APPswe/PS1dE9 transgenic AD mouse, presenting with the toxic Aβ1-42 deposition found in human AD, allowed us to characterize time-dependent changes in inflammatory and cholinergic markers present in AD. Astrogliosis was observed in cortex and hippocampus, with cellular loss occurring in the same areas in which Aβ plaques were present. In this setting, we found early significantly elevated levels of IL-1β and TNFα gene expression; with the hippocampus showing the highest IL-1β expression. To investigate the cholinergic anti-inflammatory pathway, the expression of nicotinic receptors (nAChRs) and cholinesterase enzymes also was evaluated. The anti-inflammatory nAChRα7, α4, and β2 were particularly increased at 6 months of age in the hippocampus, potentially as a strategy to counteract Aβ deposition and the ensuing inflammatory state. A time-dependent subunit switch to the α3β4 type occurred. Whether α3, β4 subunits have a pro-inflammatory or an inhibitory effect on ACh stimulation remains speculative. Aβ1-42 deposition, neuronal loss and increased astrocytes were detected, and a time-dependent change in components of the cholinergic anti-inflammatory pathway were observed. A greater understanding of time-dependent Aβ/nAChRs interactions may aid in defining new therapeutic strategies and novel molecular targets.D’Angelo ChiaraCostantini EricaSalvador NievesMarchioni MicheleDi Nicola MartaGreig H. NigelReale MarcellaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q D’Angelo Chiara Costantini Erica Salvador Nieves Marchioni Michele Di Nicola Marta Greig H. Nigel Reale Marcella nAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse
description	Abstract An evaluation of the APPswe/PS1dE9 transgenic AD mouse, presenting with the toxic Aβ1-42 deposition found in human AD, allowed us to characterize time-dependent changes in inflammatory and cholinergic markers present in AD. Astrogliosis was observed in cortex and hippocampus, with cellular loss occurring in the same areas in which Aβ plaques were present. In this setting, we found early significantly elevated levels of IL-1β and TNFα gene expression; with the hippocampus showing the highest IL-1β expression. To investigate the cholinergic anti-inflammatory pathway, the expression of nicotinic receptors (nAChRs) and cholinesterase enzymes also was evaluated. The anti-inflammatory nAChRα7, α4, and β2 were particularly increased at 6 months of age in the hippocampus, potentially as a strategy to counteract Aβ deposition and the ensuing inflammatory state. A time-dependent subunit switch to the α3β4 type occurred. Whether α3, β4 subunits have a pro-inflammatory or an inhibitory effect on ACh stimulation remains speculative. Aβ1-42 deposition, neuronal loss and increased astrocytes were detected, and a time-dependent change in components of the cholinergic anti-inflammatory pathway were observed. A greater understanding of time-dependent Aβ/nAChRs interactions may aid in defining new therapeutic strategies and novel molecular targets.
format	article
author	D’Angelo Chiara Costantini Erica Salvador Nieves Marchioni Michele Di Nicola Marta Greig H. Nigel Reale Marcella
author_facet	D’Angelo Chiara Costantini Erica Salvador Nieves Marchioni Michele Di Nicola Marta Greig H. Nigel Reale Marcella
author_sort	D’Angelo Chiara
title	nAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse
title_short	nAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse
title_full	nAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse
title_fullStr	nAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse
title_full_unstemmed	nAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse
title_sort	nachrs gene expression and neuroinflammation in appswe/ps1de9 transgenic mouse
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/c4aad8a0c7404052a401dc4f37a93ef6
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nAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse

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