Activation of the contact system in cerebrospinal fluid of patientswith Alzheimer disease
L. Bergamaschini
Bok Engelsk 1998
| Utgitt | 1998
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| Omfang | Side 102- 108
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| Opplysninger | Several converging lines of evidence suggest that beta-amyloid andinflammation may be linked in the pathogenesis of Alzheimer disease(AD), but the mechanism of beta-amyloid neurotoxicity is unclear, inthis study, by demonstrating that high molecular weight kininogen maybe massively cleaved in the cerebrospinal fluid (CSF) of patientswith AD, we provide evidence of the potential involvement of thecontact system in the inflammatory processes taking place in thisdisease. In the CSF of patients with neuroimmune inflammatory disease(multiple sclerosis, chronic inflammatory demyelinatingpolyneuropathy), there was no evidence of increased cleavage of highmolecular weight kininogen, suggesting that this finding maybecharacteristic of the Alzheimer brain. The data obtained from invitro experiments seem to indicate that the cleavage of highmolecular weight kininogen in vivo may be the result of theinteraction of beta-amyloid with factor XII and of kallikreingeneration. The actual relevance of such a phenomenon remains to beestablished in vivo. However, the demonstration that the contactsystem may be activated in the brains of Alzheimer patients points tothe potential involvement of the kallikrein-kinin system in theinflammatory process of this disease.
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