Torpor enhances synaptic strength and restores memory performance in a mouse model of Alzheimer’s disease

Abstract Hibernation induces neurodegeneration-like changes in the brain, which are completely reversed upon arousal. Hibernation-induced plasticity may therefore be of great relevance for the treatment of neurodegenerative diseases, but remains largely unexplored. Here we show that a single torpor...

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Autores principales:	Christina F. de Veij Mestdagh, Jaap A. Timmerman, Frank Koopmans, Iryna Paliukhovich, Suzanne S. M. Miedema, Maaike Goris, Rolinka J. van der Loo, Guido Krenning, Ka Wan Li, Huibert D. Mansvelder, August B. Smit, Robert H. Henning, Ronald E. van Kesteren
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/79d911a2ec34496183b119acd53c6f51
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spelling	oai:doaj.org-article:79d911a2ec34496183b119acd53c6f512021-12-02T18:47:10ZTorpor enhances synaptic strength and restores memory performance in a mouse model of Alzheimer’s disease10.1038/s41598-021-94992-x2045-2322https://doaj.org/article/79d911a2ec34496183b119acd53c6f512021-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-94992-xhttps://doaj.org/toc/2045-2322Abstract Hibernation induces neurodegeneration-like changes in the brain, which are completely reversed upon arousal. Hibernation-induced plasticity may therefore be of great relevance for the treatment of neurodegenerative diseases, but remains largely unexplored. Here we show that a single torpor and arousal sequence in mice does not induce dendrite retraction and synapse loss as observed in seasonal hibernators. Instead, it increases hippocampal long-term potentiation and contextual fear memory. This is accompanied by increased levels of key postsynaptic proteins and mitochondrial complex I and IV proteins, indicating mitochondrial reactivation and enhanced synaptic plasticity upon arousal. Interestingly, a single torpor and arousal sequence was also sufficient to restore contextual fear memory in an APP/PS1 mouse model of Alzheimer’s disease. Our study demonstrates that torpor in mice evokes an exceptional state of hippocampal plasticity and that naturally occurring plasticity mechanisms during torpor provide an opportunity to identify unique druggable targets for the treatment of cognitive impairment.Christina F. de Veij MestdaghJaap A. TimmermanFrank KoopmansIryna PaliukhovichSuzanne S. M. MiedemaMaaike GorisRolinka J. van der LooGuido KrenningKa Wan LiHuibert D. MansvelderAugust B. SmitRobert H. HenningRonald E. van KesterenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Christina F. de Veij Mestdagh Jaap A. Timmerman Frank Koopmans Iryna Paliukhovich Suzanne S. M. Miedema Maaike Goris Rolinka J. van der Loo Guido Krenning Ka Wan Li Huibert D. Mansvelder August B. Smit Robert H. Henning Ronald E. van Kesteren Torpor enhances synaptic strength and restores memory performance in a mouse model of Alzheimer’s disease
description	Abstract Hibernation induces neurodegeneration-like changes in the brain, which are completely reversed upon arousal. Hibernation-induced plasticity may therefore be of great relevance for the treatment of neurodegenerative diseases, but remains largely unexplored. Here we show that a single torpor and arousal sequence in mice does not induce dendrite retraction and synapse loss as observed in seasonal hibernators. Instead, it increases hippocampal long-term potentiation and contextual fear memory. This is accompanied by increased levels of key postsynaptic proteins and mitochondrial complex I and IV proteins, indicating mitochondrial reactivation and enhanced synaptic plasticity upon arousal. Interestingly, a single torpor and arousal sequence was also sufficient to restore contextual fear memory in an APP/PS1 mouse model of Alzheimer’s disease. Our study demonstrates that torpor in mice evokes an exceptional state of hippocampal plasticity and that naturally occurring plasticity mechanisms during torpor provide an opportunity to identify unique druggable targets for the treatment of cognitive impairment.
format	article
author	Christina F. de Veij Mestdagh Jaap A. Timmerman Frank Koopmans Iryna Paliukhovich Suzanne S. M. Miedema Maaike Goris Rolinka J. van der Loo Guido Krenning Ka Wan Li Huibert D. Mansvelder August B. Smit Robert H. Henning Ronald E. van Kesteren
author_facet	Christina F. de Veij Mestdagh Jaap A. Timmerman Frank Koopmans Iryna Paliukhovich Suzanne S. M. Miedema Maaike Goris Rolinka J. van der Loo Guido Krenning Ka Wan Li Huibert D. Mansvelder August B. Smit Robert H. Henning Ronald E. van Kesteren
author_sort	Christina F. de Veij Mestdagh
title	Torpor enhances synaptic strength and restores memory performance in a mouse model of Alzheimer’s disease
title_short	Torpor enhances synaptic strength and restores memory performance in a mouse model of Alzheimer’s disease
title_full	Torpor enhances synaptic strength and restores memory performance in a mouse model of Alzheimer’s disease
title_fullStr	Torpor enhances synaptic strength and restores memory performance in a mouse model of Alzheimer’s disease
title_full_unstemmed	Torpor enhances synaptic strength and restores memory performance in a mouse model of Alzheimer’s disease
title_sort	torpor enhances synaptic strength and restores memory performance in a mouse model of alzheimer’s disease
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/79d911a2ec34496183b119acd53c6f51
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Torpor enhances synaptic strength and restores memory performance in a mouse model of Alzheimer’s disease

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