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Astrocyte atrophy and immune dysfunction in self-harming macaques.

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Self-injurious behavior (SIB) in macaques is linked to significant changes in astrocyte morphology and immune activation. Astrocytes showed atrophy and reduced complexity, alongside increased immune marker expression.

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Area of Science:

  • Neuroscience
  • Immunology
  • Primate Behavior

Background:

  • Self-injurious behavior (SIB) presents complex neuropsychological and locomotor abnormalities.
  • Potential neuropathogenesis mechanisms involve immune dysregulation, soluble factors, and astrocyte dysfunction.

Purpose of the Study:

  • To investigate the role of astrocytes in modulating immune function in macaques exhibiting SIB.
  • To quantify changes in astrocyte morphology and function associated with SIB.

Main Methods:

  • Examined frontal cortex tissue from rhesus macaques with SIB.
  • Stained tissue for glial fibrillary acidic protein (GFAP) and Toll-like receptor 2 (TLR2).
  • Utilized computer-assisted camera lucida to analyze astrocyte morphology.

Main Results:

  • Observed white matter astrocyte cell body atrophy and reduced arbor length in both gray and white matter astrocytes.
  • Found decreased bifurcations and tips on astrocytes in macaques with SIB.
  • Detected a five-fold increase in astrocytes positive for TLR2, indicating immune activation.

Conclusions:

  • SIB is associated with significant alterations in astrocyte morphology.
  • SIB induces immune activation of astrocytes, evidenced by increased TLR2 expression.
  • These findings highlight astrocyte dysfunction as a component of SIB neuropathogenesis.