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The Role of Choroid Plexus In IVIG-induced Beta-Amyloid Clearance #MMPMID24747018
Gu H; Zhong Z; Jiang W; Du E; Dodel R; Farlow MR; Zheng W; Du Y
Neuroscience 2014[Jun]; 270 (ä): 168-76 PMID24747018show ga
We have shown that intravenous immunoglobulin (IVIG) contains anti-A? autoantibodies and IVIG could induce beta amyloid (A?) efflux from cerebrospinal fluid (CSF) to blood in both Multiple Sclerosis (MS) and Alzheimer disease (AD) patients. However, the molecular mechanism underlying IVIG-induced A? efflux remains unclear. In this study, we used amyloid precursor protein (A?PP) transgenic mice to investigate if the IVIG could induce efflux of A? from the brain and whether low-density lipoprotein receptor-related protein-1 (LRP1), a hypothetic A? transporter in blood-cerebrospinal fluid barrier (BCB); could mediate this clearance process. We currently provide strong evidence to demonstrate that IVIG could reduce brain A? levels by pulling A? into the blood system in A?PP transgenic mice. In the mechanistic study, IVIG could induce A? efflux through the in-vitro BCB membrane formed by cultured BCB epithelial cells. Both RAP (receptor-associated protein; a functional inhibitor of LRP1), and LRP1 siRNA were able to significantly inhibit the A? efflux. Should A? prove to be the underlying cause of AD, our results strongly suggest that IVIG could be beneficial in the therapy for Alzheimer's disease (AD) by inducing efflux of A? from the brain through the LRP1 in the BCB.