Interleukin-6-associated inflammatory processes in Alzheimer's disease: new therapeutic options

Neurobiol Aging. Sep-Oct 1996;17(5):795-800. doi: 10.1016/0197-4580(96)00107-8.

Abstract

The cytokine interleukin-6 is consistently detected in the brains of Alzheimer's disease patients but not in the brains of nondemented elderly persons. Until recently it was unclear whether an interleukin-6-associated inflammatory mechanism is an early or late event in the pathological cascade of Alzheimer's disease. We investigated whether interleukin-6 could be detected in plaques of Alzheimer's disease patients prior to the onset of neuritic degeneration. We found interleukin-6 mostly in plaques where neuritic pathology has not yet developed. This indicates that the appearance of interleukin-6 may precede neuritic changes and is not just a consequence of neuritic degeneration. Therefore, one may hypothesize that activation of inflammatory mechanisms may cause neuritic degeneration in plaques. A suppression of interleukin-6 synthesis could, therefore, be of therapeutic value. Upon screening a number of substances, we found that a small number of nonsteroidal antiinflammatory drugs, including tenidap, were able to inhibit interleukin-6 synthesis in cultured human astrocytoma cells. These substances may be therapeutically useful in Alzheimer's disease and should be evaluated in clinical studies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology*
  • Alzheimer Disease / therapy
  • Astrocytoma / metabolism
  • Brain / pathology
  • Brain Chemistry / physiology
  • Brain Neoplasms / metabolism
  • Humans
  • Inflammation / metabolism
  • Inflammation / pathology*
  • Inflammation / therapy
  • Interleukin-6 / biosynthesis
  • Interleukin-6 / metabolism
  • Interleukin-6 / physiology*
  • Nerve Degeneration / physiology
  • Neurites / physiology
  • Neurofibrillary Tangles / pathology
  • Tumor Cells, Cultured

Substances

  • Interleukin-6