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Chronic stress as a risk factor for Alzheimer's disease: Roles of microglia-mediated synaptic remodeling,

Kanchan Bisht1, Kaushik Sharma1, Marie-Ève Tremblay1,2

  • 1Axe Neurosciences, CRCHU de Québec-Université Laval, Québec, QC, Canada.

Neurobiology of Stress
|July 12, 2018
PubMed

Insights

Chronic stress impacts microglia, the brain's immune cells, increasing Alzheimer's disease (AD) risk. Understanding these stress-modulated microglial functions offers new therapeutic targets for AD.

Area of Science:

  • Neuroscience
  • Immunology
  • Neurodegenerative Diseases

Background:

  • Microglia are central nervous system (CNS) immune cells vital for homeostasis, synaptic plasticity, learning, and memory.
  • Chronic stress is a significant risk factor for neurodegenerative diseases like Alzheimer's disease (AD).
  • Microglia play complex roles in AD, contributing to pathology (Aβ accumulation, tau tangles) and potentially offering neuroprotection (Aβ phagocytosis).

Purpose of the Study:

  • To review the intricate relationship between chronic stress and Alzheimer's disease (AD) pathology.
  • To elucidate the multifaceted roles of microglia in AD pathogenesis.
  • To highlight stress-induced microglial phenotypes and their potential for neuroprotection in AD.

Main Methods:

  • Literature review focusing on the interplay between chronic stress, microglial function, and AD.
  • Analysis of current research on microglial phenotypes in the context of stress and AD.
  • Synthesis of findings to identify therapeutic opportunities.

Main Results:

  • Chronic stress significantly modulates microglial functions, influencing AD risk and progression.
  • Specific microglial phenotypes associated with both neuroprotection and neurodegeneration under chronic stress and AD conditions have been identified.
  • These phenotypes offer insights into the dual role of microglia in AD.

Conclusions:

  • Chronic stress is a critical environmental factor influencing microglial activity in AD.
  • Targeting stress-modulated microglial phenotypes presents a promising avenue for developing novel AD therapeutics.
  • Further research into these specific microglial states could lead to more effective interventions for AD patients.
Keywords:
ABCA7, ATP-binding cassette transporter A7AD, Alzheimer's diseaseAPOE, Apolipoprotein EAPP, amyloid precursor proteinAlzheimer's diseaseAβ, Amyloid betaBDNF, brain derived neurotrophic factorCD11b, cluster of differentiation molecule 11BCD33, cluster of differentiation 33CNS, central nervous systemCR, complement receptorCRF, corticotropin releasing factorDAM, disease associated microgliaDAP12, DNAX-activation protein 12Dark microgliaFAD, Familial Alzheimer's diseaseFCRLS, Fc receptor-like S scavenger receptorGR, glucocorticoid receptorHPA axis, hypothalamic pituitary adrenocortical axisIBA1, ionized calcium-binding adapter molecule 1IL, interleukinLTP, long-term potentiationMGnD, microglia with a neurodegenerative phenotypeMR, mineralocorticoid receptorMicrogliaMicroglial phenotypesNADPH, nicotinamide adenine dinucleotide phosphateNFT, neurofibrillary tanglesNeurodegenerationNeuroinflammationPS, presenilinROS, reactive oxygen speciesStressSynaptic remodelingTGFβ, transforming growth factor βTLR, Toll-like receptorsTMEM119, transmembrane protein 119TNFα, tumor necrosis factor-αTREM2, triggering receptor expressed in myeloid cells 2TYROBP, TYRO protein tyrosine kinase binding proteinmPFC, medial prefrontal cortex

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