Cited by 87Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

Microglia communication: parallels between aging and Alzheimer's disease

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Udeochu, Joe C., Shea, Jeremy M., Villeda, Saul A.·2016·Clinical and Experimental Neuroimmunology

Abstract

Aging alters the functional integrity of the adult brain, driving cognitive impairments and susceptibility to neurodegenerative disorders in healthy individuals. In fact, aging remains the most dominant risk factor for Alzheimer's disease (AD). Recent findings have expanded our understanding of microglia function in the normal aging and AD brain, provoking an appreciation for microglia involvement in remodeling neuronal connections and maintaining brain integrity. This homeostatic function of microglia is achieved in part through the ability of microglia to interact extensively with and rapidly respond to changes in the brain microenvironment to enable adequate phenotypic transformations. Here, we discuss pro-inflammatory drivers of microglia transformation in aging and AD by focusing on the immune-modulatory functions of secreted factors, such as cytokines, complement factors and extracellular vesicles. We highlight the involvement of these secreted factors in aging and AD-associated cellular changes in microglia immune activation, surveillance function, and phagocytosis. Finally, we discuss how pro-inflammatory phenotypic changes associated with altered immune communication could both facilitate and exacerbate impairments in synaptic plasticity and cognitive function observed in the aged and AD brain.

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  • Both inflammation and reduced microglial phagocytic capacity in AD can contribute to the decline in synaptic plasticity observed in this pathology.

    “Both inflammation and reduced microglial phagocytic capacity in AD can contribute to the decline in synaptic plasticity observed in this pathology (Ritzel et al., 2015; Udeochu et al., 2016).”
  • Aged microglia show reduced phagocytic capacity, which could be due partly to a reduction in the ability of microglia to recognize phagocytic targets.

    “In addition, aged microglia show reduced phagocytic capacity. This process could be due partly to a reduction in the ability of microglia to recognize phagocytic targets (Udeochu et al., 2016).”

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Authors
Udeochu, J. C., Shea, J. M., & Villeda, S. A.
Affiliations
University of California, San Francisco (US)
Corresponding author
Villeda, Saul A.
Venue
Clinical and Experimental Neuroimmunology
Publisher
Wiley
Published
2016-05
Volume
7
Issue
2
Pages
114-125
ISSN
1759-1961 (ISSN-L)
OpenAlex
W2345372985
Cited by
87
References
107
Citations by year
2026: 3 · 2025: 9 · 2024: 12 · 2023: 4 · 2022: 7 · 2021: 12 · 2020: 8 · 2019: 7 · 2018: 8 · 2017: 16 · 2016: 1
FWCI
0.93
Type
journal article
Language
en
Open access
Locations
  • Clinical and Experimental Neuroimmunology (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
  • National Science Foundation
  • Sandler Foundation
  • National Institutes of Health (DP5‐OD12178)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
microglia, aging, Alzheimer's disease, microglial activation, neuroinflammation, cytokines, complement system, extracellular vesicles, phagocytosis, microglial surveillance, synaptic plasticity, cognitive impairment, neurodegeneration

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