Inflammation and Alzheimer disease
Paul S. Aisen
Bok Engelsk 1996
| Utgitt | 1996
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|---|---|
| Omfang | Side 83- 88
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| Opplysninger | Inflammatory mechanisms are active in patients with Alzheimerdisease. Serum elevations of acute phase proteins such as alpha 1-antichymotrypsin, along with deposition of inflammatory cytokines inthe brain, suggest a ''cerebral acute phase response'' contributingto amyloid deposition and tissue destruction. Activated microgliapossessing HLA-DR surface markers accumulate around amyloid plaques.The complement cascade leads to generation of the membrane attackcomplex, which may directly damage neuronal membranes. This growingbody of evidence suggests that empirical trials of anti-inflammatorydrugs are now appropriate to test the hypothesis that suppression ofthese mechanisms will slow the rate of progression of Alzheimerdisease. Several drugs useful in the treatment of rheumatic diseasesare candidates for study in Alzheimer disease, includingglucocorticoids, antimalarial drugs, and colchicine. Pilot studies ofthe synthetic glucocorticoid prednisone indicate that treatment witha moderate dose is well tolerated in patients with Alzheimer disease,and suppresses serum levels of acute phase proteins. Based on thisexperience, a multicenter parallel-design placebo-controlled trialhas been initiated with the Alzheimer's Disease Cooperative Study todetermine whether treatment with prednisone can slow the rate ofprogression of Alzheimer disease.
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| Emner |
