Psychological Stress as a Risk Factor for Accelerated Cellular Aging and Cognitive Decline: The Involvement of Microglia-Neuron Crosstalk

The relationship between the central nervous system (CNS) and microglia is lifelong. Microglia originate in the embryonic yolk sac during development and populate the CNS before the blood-brain barrier forms. In the CNS, they constitute a self-renewing population. Although they represent up to 10% o...

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Autores principales:	Micaël Carrier, Eva Šimončičová, Marie-Kim St-Pierre, Chloe McKee, Marie-Ève Tremblay
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	microglia neuron synapse cognitive aging oxidative stress chronic psychological stress Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
Acceso en línea:	https://doaj.org/article/2d93b160c13d4237b548acda9da794ad
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spelling	oai:doaj.org-article:2d93b160c13d4237b548acda9da794ad2021-11-04T06:00:12ZPsychological Stress as a Risk Factor for Accelerated Cellular Aging and Cognitive Decline: The Involvement of Microglia-Neuron Crosstalk1662-509910.3389/fnmol.2021.749737https://doaj.org/article/2d93b160c13d4237b548acda9da794ad2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fnmol.2021.749737/fullhttps://doaj.org/toc/1662-5099The relationship between the central nervous system (CNS) and microglia is lifelong. Microglia originate in the embryonic yolk sac during development and populate the CNS before the blood-brain barrier forms. In the CNS, they constitute a self-renewing population. Although they represent up to 10% of all brain cells, we are only beginning to understand how much brain homeostasis relies on their physiological functions. Often compared to a double-edged sword, microglia hold the potential to exert neuroprotective roles that can also exacerbate neurodegeneration once compromised. Microglia can promote synaptic growth in addition to eliminating synapses that are less active. Synaptic loss, which is considered one of the best pathological correlates of cognitive decline, is a distinctive feature of major depressive disorder (MDD) and cognitive aging. Long-term psychological stress accelerates cellular aging and predisposes to various diseases, including MDD, and cognitive decline. Among the underlying mechanisms, stress-induced neuroinflammation alters microglial interactions with the surrounding parenchymal cells and exacerbates oxidative burden and cellular damage, hence inducing changes in microglia and neurons typical of cognitive aging. Focusing on microglial interactions with neurons and their synapses, this review discusses the disrupted communication between these cells, notably involving fractalkine signaling and the triggering receptor expressed on myeloid cells (TREM). Overall, chronic stress emerges as a key player in cellular aging by altering the microglial sensome, notably via fractalkine signaling deficiency. To study cellular aging, novel positron emission tomography radiotracers for TREM and the purinergic family of receptors show interest for human study.Micaël CarrierMicaël CarrierEva ŠimončičováMarie-Kim St-PierreMarie-Kim St-PierreChloe McKeeChloe McKeeMarie-Ève TremblayMarie-Ève TremblayMarie-Ève TremblayMarie-Ève TremblayMarie-Ève TremblayFrontiers Media S.A.articlemicroglianeuronsynapsecognitive agingoxidative stresschronic psychological stressNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENFrontiers in Molecular Neuroscience, Vol 14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	microglia neuron synapse cognitive aging oxidative stress chronic psychological stress Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
spellingShingle	microglia neuron synapse cognitive aging oxidative stress chronic psychological stress Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Micaël Carrier Micaël Carrier Eva Šimončičová Marie-Kim St-Pierre Marie-Kim St-Pierre Chloe McKee Chloe McKee Marie-Ève Tremblay Marie-Ève Tremblay Marie-Ève Tremblay Marie-Ève Tremblay Marie-Ève Tremblay Psychological Stress as a Risk Factor for Accelerated Cellular Aging and Cognitive Decline: The Involvement of Microglia-Neuron Crosstalk
description	The relationship between the central nervous system (CNS) and microglia is lifelong. Microglia originate in the embryonic yolk sac during development and populate the CNS before the blood-brain barrier forms. In the CNS, they constitute a self-renewing population. Although they represent up to 10% of all brain cells, we are only beginning to understand how much brain homeostasis relies on their physiological functions. Often compared to a double-edged sword, microglia hold the potential to exert neuroprotective roles that can also exacerbate neurodegeneration once compromised. Microglia can promote synaptic growth in addition to eliminating synapses that are less active. Synaptic loss, which is considered one of the best pathological correlates of cognitive decline, is a distinctive feature of major depressive disorder (MDD) and cognitive aging. Long-term psychological stress accelerates cellular aging and predisposes to various diseases, including MDD, and cognitive decline. Among the underlying mechanisms, stress-induced neuroinflammation alters microglial interactions with the surrounding parenchymal cells and exacerbates oxidative burden and cellular damage, hence inducing changes in microglia and neurons typical of cognitive aging. Focusing on microglial interactions with neurons and their synapses, this review discusses the disrupted communication between these cells, notably involving fractalkine signaling and the triggering receptor expressed on myeloid cells (TREM). Overall, chronic stress emerges as a key player in cellular aging by altering the microglial sensome, notably via fractalkine signaling deficiency. To study cellular aging, novel positron emission tomography radiotracers for TREM and the purinergic family of receptors show interest for human study.
format	article
author	Micaël Carrier Micaël Carrier Eva Šimončičová Marie-Kim St-Pierre Marie-Kim St-Pierre Chloe McKee Chloe McKee Marie-Ève Tremblay Marie-Ève Tremblay Marie-Ève Tremblay Marie-Ève Tremblay Marie-Ève Tremblay
author_facet	Micaël Carrier Micaël Carrier Eva Šimončičová Marie-Kim St-Pierre Marie-Kim St-Pierre Chloe McKee Chloe McKee Marie-Ève Tremblay Marie-Ève Tremblay Marie-Ève Tremblay Marie-Ève Tremblay Marie-Ève Tremblay
author_sort	Micaël Carrier
title	Psychological Stress as a Risk Factor for Accelerated Cellular Aging and Cognitive Decline: The Involvement of Microglia-Neuron Crosstalk
title_short	Psychological Stress as a Risk Factor for Accelerated Cellular Aging and Cognitive Decline: The Involvement of Microglia-Neuron Crosstalk
title_full	Psychological Stress as a Risk Factor for Accelerated Cellular Aging and Cognitive Decline: The Involvement of Microglia-Neuron Crosstalk
title_fullStr	Psychological Stress as a Risk Factor for Accelerated Cellular Aging and Cognitive Decline: The Involvement of Microglia-Neuron Crosstalk
title_full_unstemmed	Psychological Stress as a Risk Factor for Accelerated Cellular Aging and Cognitive Decline: The Involvement of Microglia-Neuron Crosstalk
title_sort	psychological stress as a risk factor for accelerated cellular aging and cognitive decline: the involvement of microglia-neuron crosstalk
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/2d93b160c13d4237b548acda9da794ad
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Psychological Stress as a Risk Factor for Accelerated Cellular Aging and Cognitive Decline: The Involvement of Microglia-Neuron Crosstalk

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