Long-term intracerebral inflammatory response after traumatic brain injury

Forensic Sci Int. 2004 Dec 16;146(2-3):97-104. doi: 10.1016/j.forsciint.2004.06.027.

Abstract

Epidemiological and pathological studies suggest that head injury is a significant risk factor for subsequent neurodegeneration and cognitive decline in later life. The precise mechanisms for the development of post-traumatic neurodegenerative change are unclear but we hypothesize that persistence of inflammatory processes in the brain may play a key role and that some individuals are more susceptible to such changes based on their genetic make-up. In support of this hypothesis we present evidence of persistent elevated microglial activity in long-term survivors of head injury and the suggestion of an association between the extent of this activity and interleukin-1 genotype.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Alleles
  • Antigens, CD / metabolism
  • Antigens, Differentiation, Myelomonocytic / metabolism
  • Apolipoproteins E / genetics
  • Biomarkers / metabolism
  • Brain / metabolism
  • Brain / pathology*
  • Brain Injuries / metabolism
  • Brain Injuries / pathology*
  • Case-Control Studies
  • Child
  • Child, Preschool
  • Female
  • Forensic Pathology
  • Genotype
  • Humans
  • Hyperplasia / metabolism
  • Hypertrophy / metabolism
  • Infant
  • Inflammation / metabolism
  • Inflammation / pathology*
  • Interleukin-1 / genetics
  • Interleukin-1 / metabolism
  • Macrophage-1 Antigen / metabolism
  • Male
  • Microglia / metabolism
  • Microglia / pathology*
  • Middle Aged
  • Phagocytosis
  • Survival Analysis

Substances

  • Antigens, CD
  • Antigens, Differentiation, Myelomonocytic
  • Apolipoproteins E
  • Biomarkers
  • CD68 antigen, human
  • Interleukin-1
  • Macrophage-1 Antigen