ABSTRACT
Alzheimer's disease (AD) is a neurodegenerative disease caused by accumulation of amyloid beta (Aß) plaque and neurofibrillary tangle formation. We have shown in vitro, that knock-down and blockade of the 37 kDa/67 kDa Laminin Receptor (LRP/LR) resulted in reduced Aß induced cytotoxicity and Aß accumulation. In order to test the effect of blocking LRP/LR on Aß formation and AD associated symptoms, AD transgenic mice received the anti-LRP/LR specific antibody, IgG1-iS18 through intranasal administration. We show that this treatment resulted in an improvement in memory, and decreased Aß plaque formation. Moreover, a significant decrease in Aß42 protein expression with a concomitant increase in amyloid precursor protein (APP) and telomerase reverse transcriptase (mTERT) levels was observed. These data recommend IgG1-iS18 as a potentially powerful therapeutic antibody for AD treatment.
