Activation of the contact system in cerebrospinal fluid of patients with Alzheimer disease

Luigi Bergamaschini, Lucilla Parnetti, Davide Pareyson, Stefania Canziani, Massimo Cugno, Angelo Agostoni

Research output: Contribution to journalArticlepeer-review

Abstract

Several converging lines of evidence suggest that β-amyloid and inflammation may be linked in the pathogenesis of Alzheimer disease (AD), but the mechanism of β-amyloid neurotoxicity is unclear. In this study, by demonstrating that high molecular weight kininogen may be massively cleaved in the cerebrospinal fluid (CSF) of patients with AD, we provide evidence of the potential involvement of the contact system in the inflammatory processes taking place in this disease. In the CSF of patients with neuroimmune inflammatory disease (multiple sclerosis, chronic inflammatory demyelinating polyneuropathy), there was no evidence of increased cleavage of high molecular weight kininogen, suggesting that this finding may be characteristic of the Alzheimer brain. The data obtained from in vitro experiments seem to indicate that the cleavage of high molecular weight kininogen in vivo may be the result of the interaction of β-amyloid with factor XII and of kallikrein generation. The actual relevance of such a phenomenon remains to be established in vivo. However, the demonstration that the contact system may be activated in the brains of Alzheimer patients points to the potential involvement of the kallikrein-kinin system in the inflammatory process of this disease.

Original languageEnglish
Pages (from-to)102-108
Number of pages7
JournalAlzheimer Disease and Associated Disorders
Volume12
Issue number2
Publication statusPublished - 1998

Keywords

  • Contact system
  • Factor XII
  • High molecular weight kininogen
  • Inflammation
  • Kallikrein
  • β-Amyloid

ASJC Scopus subject areas

  • Geriatrics and Gerontology
  • Psychiatry and Mental health
  • Neuroscience(all)

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