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

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*

*Bijbehorende auteur voor dit werk

OnderzoeksoutputAcademicpeer review

5 Citaten (Scopus)
123 Downloads (Pure)


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.

Originele taal-2English
Aantal pagina's13
TijdschriftScientific Reports
Nummer van het tijdschrift1
StatusPublished - 29-jul.-2021

Citeer dit