Evidence for the involvement of inflammatory processes in the pathogenesis of 
Alzheimer's disease (AD) has been documented for a long time. However, the 
inflammation hypothesis in relation to AD pathology has emerged relatively 
recently. Even in this hypothesis, the inflammatory reaction is still considered 
to be a downstream effect of the accumulated proteins (amyloid beta (Abeta) and 
tau). This review aims to highlight the importance of the immune processes 
involved in AD pathogenesis based on the outcomes of the two major 
inflammation-relevant treatment strategies against AD developed and tested to 
date in animal studies and human clinical trials - the use of anti-inflammatory 
drugs and immunisation against Abeta.