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Astrocyte Circadian Timekeeping in Brain Health and Neurodegeneration

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Circadian Clock in Brain Health and Disease

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 1344))

Abstract

Almost three decades ago, astrocytes neighbouring clock neurons of the suprachiasmatic nucleus, the hypothalamic tissue responsible for synchronising circadian timekeeping in mammals, were found to undergo morphological and protein expression changes in a cyclic 24-h pattern, suggesting that glia could harbour circadian timekeeping mechanisms and that neuron–glia interactions could play a part in the daily organisation of rhythms of physiology and behaviour. Recently, it has become clear that astrocytes are circadian timekeepers, capable of initiating daily patterns of behaviour and imposing their intrinsic circadian tempo in mammals. In this chapter, we will describe properties of intracellular timekeeping of astrocytes and the mechanisms by which astrocytes functionally integrate in brain circuits underlying circadian, sleep, and cognitive behaviours in mammals. We will then discuss how altered astrocyte timekeeping may be involved in early brain vulnerability underpinning neurodegeneration. We will focus on Alzheimer’s disease as a template of how altered astrocyte timekeeping may be involved in neurodegeneration, both directly via unbalancing of inflammatory and oxidative stress cellular pathways, and indirectly, by altering sleep and cognitive functions.

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Acknowledgements

Figures created with BioRender.com. This work is supported by the UK Dementia Research Institute which receives its funding from UK DRI Ltd, funded by the UK Medical Research Council, Alzheimer’s Society and Alzheimer’s Research UK. NN was also supported by an Imperial College President’s PhD Scholarship.

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Correspondence to Marco Brancaccio .

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Brancaccio, M., Wolfes, A.C., Ness, N. (2021). Astrocyte Circadian Timekeeping in Brain Health and Neurodegeneration. In: Engmann, O., Brancaccio, M. (eds) Circadian Clock in Brain Health and Disease. Advances in Experimental Medicine and Biology, vol 1344. Springer, Cham. https://doi.org/10.1007/978-3-030-81147-1_6

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