Abstract

Background: Amyloid-beta peptide (A beta) deposition in Alzheimer's disease (AD) is due to an imbalance in its production/clearance rate. Ap is transported across the blood-brain barrier by LRP1 and P-gp as efflux transporters and RAGE as influx transporter. Vitamin D deficit and polymorphisms of the vitamin D receptor (VDR) gene are associated with high prevalence of mild cognitive impairment (MCI) and AD. Further, vitamin D promotes the expression of LRP1 and P-gp in AD-animal model brains.