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

Micaël Carrier1,2, Eva Šimončičová2, Marie-Kim St-Pierre2,3

  • 1Axe Neurosciences, Centre de Recherche du CHU de Québec, Université Laval, Québec City, QC, Canada.

Frontiers in Molecular Neuroscience
|November 22, 2021
PubMed

Insights

Chronic stress accelerates brain aging by altering microglia, the immune cells of the central nervous system (CNS). This disrupts neuronal communication, impacting cognitive function and potentially leading to major depressive disorder (MDD).

Area of Science:

  • Neuroscience
  • Immunology
  • Cellular Biology

Background:

  • Microglia, the resident immune cells of the central nervous system (CNS), originate early in development and maintain brain homeostasis.
  • These cells act as a double-edged sword, capable of neuroprotection but also exacerbating neurodegeneration when compromised.
  • Synaptic loss, a hallmark of cognitive decline, major depressive disorder (MDD), and aging, is influenced by microglial activity.

Purpose of the Study:

  • To review the lifelong relationship between the CNS and microglia.
  • To examine how chronic psychological stress impacts microglial function and contributes to cellular aging and neuroinflammation.
  • To discuss disrupted microglial-neuronal communication, focusing on fractalkine and TREM signaling in the context of stress and aging.

Main Methods:

  • Literature review focusing on microglial function, neuroinflammation, and cellular aging.
  • Analysis of mechanisms linking chronic stress to altered microglial sensomes and neuronal interactions.
  • Discussion of potential imaging biomarkers for studying cellular aging in humans.

Main Results:

  • Chronic stress induces neuroinflammation, oxidative burden, and cellular damage, altering microglia and neurons in ways that mimic cognitive aging.
  • Stress-induced changes in microglia disrupt communication with neurons, particularly through fractalkine signaling deficiency.
  • Altered microglial sensomes due to chronic stress are implicated in accelerated cellular aging.

Conclusions:

  • Chronic stress is a significant factor in cellular aging, primarily by altering microglial function and sensomes, especially via fractalkine signaling.
  • Disrupted communication between microglia and neurons, involving pathways like fractalkine and TREM, contributes to cognitive decline and MDD.
  • Novel PET radiotracers targeting TREM and purinergic receptors offer promising avenues for studying cellular aging in humans.
Keywords:
chronic psychological stresscognitive agingmajor depressive disordermicroglianeuronoxidative stresssynapse

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