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Related Experiment Videos

Dystrophic microglia in the aging human brain.

Wolfgang J Streit1, Nicole W Sammons, Amanda J Kuhns

  • 1Department of Neuroscience, PO Box 100244, University of Florida College of Medicine, Building 59, 100 Newell Drive, Gainesville, FL 32610, USA. streit@mbi.ufl.edu

Glia
|January 20, 2004
PubMed
Summary

Microglial dystrophy, characterized by cytoplasmic abnormalities, increases with age in nondemented individuals. This suggests microglial cell senescence may contribute to age-related cognitive decline.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Aging Research

Background:

  • Microglia are the primary immune cells of the central nervous system.
  • Microglial morphology changes during activation, but age-related changes are less understood.
  • Previous studies have not extensively characterized age-associated microglial structural alterations.

Purpose of the Study:

  • To investigate microglial morphology in the aging human cerebral cortex.
  • To identify and characterize novel age-related microglial structural abnormalities.
  • To determine if these abnormalities are linked to cellular senescence.

Main Methods:

  • High-resolution LN-3 immunohistochemistry was used to examine microglial cytoplasmic structure.
  • Morphological abnormalities were identified and quantified in nondemented subjects of different ages.

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  • Changes were compared to known microglial activation states.

    • Main Results:

    • Several microglial cytoplasmic abnormalities, including deramification, spheroid formation, gnarling, and process fragmentation, were observed.
    • These identified changes were distinct from microglial activation morphology and were termed 'microglial dystrophy'.
    • Dystrophic changes were significantly more prevalent in the older subject (68 years) compared to the younger subject (38 years).

    Conclusions:

    • Microglial dystrophy represents a form of microglial cell senescence.
    • Microglial senescence is a potential factor in age-related cognitive function decline.
    • Further research into microglial senescence is warranted to understand cognitive aging.