Cited by 319Neuroinflammation and Neurodegeneration MechanismsNeurogenesis and neuroplasticity mechanismsNeurological Disease Mechanisms and Treatments

Homeostatic and injury‐induced microglia behavior in the aging brain

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Hefendehl, Jasmin K., Neher, Jonas J., Sühs, Rafael B., Kohsaka, Shinichi, Skodras, Angelos, Jucker, Mathias·2014·Aging Cell

Abstract

Summary: Microglia cells are essential for brain homeostasis and have essential roles in neurodegenerative diseases. Aging is the main risk factor for most neurodegenerative diseases, and age‐related changes in microglia may contribute to the susceptibility of the aging brain to dysfunction and neurodegeneration. We have analyzed morphology and dynamic behavior of neocortical microglia in their physiological environment in young adult (3‐month‐old), adult (11‐ to 12‐month‐old), and aged (26‐ to 27‐month‐old) C57BL/6J‐Iba1‐ eGFP mice using in vivo 2‐photon microscopy. Results show that surveying microglial cells in the neocortex exhibit age‐related soma volume increase, shortening of processes, and loss of homogeneous tissue distribution. Furthermore, microglial process speed significantly decreased with age. While only a small population of microglia showed soma movement in adult mice, the microglia population with soma movement was increased in aged mice. However, in response to tissue injury, the dynamic microglial response was age‐dependently diminished. These results provide novel insights into microglial behavior and indicate that microglial dysfunction in the aging brain may contribute to age‐related cognitive decline and neurodegenerative diseases.

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Crossref · 10.1111/acel.12149

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  • Aging microglia display signs of dystrophy, including reduced ramification and short, tortuous, swollen processes, and their ability to survey the brain and respond to insults declines with aging.

    “However, aging microglia display signs of dystrophy, including reduced ramification and short, tortuous, swollen processes (58). The ability of microglia to survey the brain and respond to insults also declines with aging (59).”

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Authors
Hefendehl, J. K., Neher, J. J., Sühs, R. B., Kohsaka, S., Skodras, A., & Jucker, M.
Affiliations
  • Hertie Institute for Clinical Brain Research (DE)
  • National Institute of Neuroscience (JP)
  • German Center for Neurodegenerative Diseases (DE)
Corresponding author
  • Hefendehl, Jasmin K.
  • Jucker, Mathias
Venue
Aging Cell
Publisher
Wiley
Published
2013-09-18
Volume
13
Issue
1
Pages
60-69
ISSN
  • 1474-9718 (ISSN-L)
  • 1474-9726
OpenAlex
W2097971052
Cited by
319
References
45
Citations by year
2026: 17 · 2025: 20 · 2024: 26 · 2023: 19 · 2022: 28 · 2021: 43 · 2020: 25 · 2019: 35 · 2018: 21 · 2017: 27 · 2016: 27 · 2015: 17 · 2014: 14
FWCI
10.69
Type
journal article
Language
en
Open access
Locations
  • Aging Cell (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • DZNE Pub (submittedVersion, cc-by)
Funders
Japan Society for the Promotion of Science
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
microglia, brain aging, microglial morphology, age-related cognitive decline, neurodegenerative diseases, tissue injury response, neocortex, microglial dysfunction
MeSH terms
Aging, Animals, Brain, Brain Injuries, Cell Movement, Homeostasis, Lasers, Mice, Inbred C57BL, Microglia, Imaging, Three-Dimensional, Cell Shape, Mice

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