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
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Research Support, N.I.H., Extramural
MeSH terms
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Adolescent
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Adult
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Aged
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Alleles
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Antigens, CD / metabolism
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Antigens, Differentiation, Myelomonocytic / metabolism
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Apolipoproteins E / genetics
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Biomarkers / metabolism
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Brain / metabolism
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Brain / pathology*
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Brain Injuries / metabolism
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Brain Injuries / pathology*
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Case-Control Studies
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Child
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Child, Preschool
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Female
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Forensic Pathology
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Genotype
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Humans
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Hyperplasia / metabolism
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Hypertrophy / metabolism
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Infant
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Inflammation / metabolism
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Inflammation / pathology*
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Interleukin-1 / genetics
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Interleukin-1 / metabolism
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Macrophage-1 Antigen / metabolism
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Male
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Microglia / metabolism
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Microglia / pathology*
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Middle Aged
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Phagocytosis
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Survival Analysis
Substances
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Antigens, CD
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Antigens, Differentiation, Myelomonocytic
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Apolipoproteins E
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Biomarkers
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CD68 antigen, human
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Interleukin-1
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Macrophage-1 Antigen