[Inflammatory mechanisms in the pathogenesis of Alzheimer's disease]

Senile plaques belong to the pathological hallmarks of the brains of patients with Alzheimer's disease. There is an increasing amount of evidence that the formation of senile plaques is accompanied by an acute phase reaction, involving the production of several inflammation-associated proteins and the activation of microglial cells. The products of these inflammatory reactions may contribute to the fibrillogenesis of the amyloid beta protein, the major constituent of senile plaques. Both fibrils of the amyloid beta protein and products of activated microglial cells may be neurotoxic, leading to neuronal degeneration and to clinical symptoms of dementia. Recent epidemiological findings have drawn attention to the possibility of therapy with anti-inflammatory agents. Although the results of these studies suggest a beneficial effect of such therapy, further study is warranted to gain more insight into the fundamental aspects of such treatment as well as to develop specific drugs that have little side-effects.