Microglial interleukin-1 alpha expression in human head injury: correlations with neuronal and neuritic beta-amyloid precursor protein expression

Neurosci Lett. 1994 Aug 1;176(2):133-6. doi: 10.1016/0304-3940(94)90066-3.

Abstract

Activated microglia containing IL-1 alpha-immunoreactive (IL-1 alpha +) product were increased 3-fold in number in the acute phase following head injury, a risk factor for later development of Alzheimer's disease, and this increase was correlated with a 7-fold increase in the number of neurons with elevated beta-amyloid precursor protein (beta-APP) levels (R = 0.78; P < 0.05). Furthermore, clusters of beta-APP+ dystrophic neurites present in these patients were invariably associated with activated IL-1 alpha + microglia. These findings suggest that early overexpression of IL-1 alpha and beta-APP is a priming event for later neuropathological changes evident at end stages of Alzheimer's disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Aged
  • Amyloid beta-Protein Precursor / biosynthesis*
  • Craniocerebral Trauma / metabolism*
  • Female
  • Glial Fibrillary Acidic Protein / metabolism
  • Humans
  • Immunohistochemistry
  • Interleukin-1 / biosynthesis*
  • Male
  • Microglia / metabolism*
  • Middle Aged
  • Nerve Regeneration / physiology
  • Neurites / metabolism*
  • Neurons / metabolism*

Substances

  • Amyloid beta-Protein Precursor
  • Glial Fibrillary Acidic Protein
  • Interleukin-1