Inflammatory mechanisms in the brain may contribute to the neurodegene
rative process in Alzheimer's disease. The cerebral acute-phase respon
se mediated by inflammatory cytokines, the complement cascade, and the
accumulation of activated microglial cells are appropriate targets fo
r anti-inflammatory intervention. Pilot studies showed that tolerable
doses of prednisone suppress the peripheral acute-phase response in Al
zheimer's disease, and a multicenter therapeutic trial of prednisone i
s in progress. Two other anti-inflammatory drugs, hydroxychloroquine a
nd colchicine, are also under investigation.