Inflammatory processes develop in the vicinity of the neuropathological hal
lmarks associated with Alzheimer's disease (AD) and may play a role in the
progression of the disease and its clinical expression. We have previously
reported that chronic infusion of LPS into the fourth ventricle of rat brai
ns reproduced many of the inflammatory and pathological changes seen in the
brain of AD patients. In the current study, we used the same animal model
to investigate the effects of longer infusion of LPS and whether these effe
cts could recover over time. The results show that doubling the time of LPS
infusion did not increased the inflammatory reaction and did not produce a
significantly greater behavioral impairment. Waiting for 37 days after the
cessation of the LPS infusion did not decrease the density of activated mi
croglia and did not improve performances in the Morris water maze task. The
results suggest that inflammation may contribute to the pathogenic mechani
sms that underlie the clinical expression of AD. NeuroReport 11:1759-1763 (
C) 2000 Lippincott Williams & Wilkins.