Strategies to delay the onset of Alzheimer's disease.
Several processes are implicated in the neuropathology of Alzheimer's disease (AD), such as the deposition of amyloid, the formation of paired helical filaments and the proinflammatory activation of microglial and astroglial cells. Proinflammatory activation of glial cells has been a focus of research for a mere ten years now. However, the availability of and broad experience with anti-inflammatory drugs has led to several ongoing clinical trials to verify the capacity of anti-inflammatory drugs to ameliorate the deterioration in AD. The enzymatic cleavage of the amyloid-precursor-protein or the hyperphosphorylation of tau as well as the subsequent aggregation of the resulting products are further targets for drugs intended to delay the neuropathological destruction observed in AD.
Hüll
M H
MH
Dept. of Psychiatry, University of Freiburg, Germany.
Fiebich
B L
BL
Lieb
K
K
D000368:Aged; D000544:Alzheimer Disease / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D000682:Amyloid / Q000378:metabolism; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D002799:Cholinergic Fibers / Q000473:pathology; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology; D006801:Humans; D007249:Inflammation / Q000473:pathology; D009154:Mutation; D016874:Neurofibrillary Tangles / Q000378:metabolism / Q000473:pathology; D012307:Risk Factors
D000682:Amyloid; D000894:Anti-Inflammatory Agents, Non-Steroidal; D002800:Cholinesterase Inhibitors; D004967:Estrogens