A Connectivity between LRP-1 and Alzheimer’s Disease: Modulating the Transport and Clearance of Tau and Aβ Clearance from the Brain to the Liver

Authors: Tackett AN and Duffy L*

DOI: 10.23880/act-16000281

Volume 8, Issue 4

Abstract

A paucity of knowledge exists in our understanding of the axonal clearance of both beta amyloid (Aβ) and Tau proteins to the liver. Peripheral clearance by the liver can remove 40–50% of Aβ burden in the brain through the glial-lymphatic (glymphatic) system, transport across the blood brain barrier and mediated by low-density lipoprotein receptor-related peptide 1 (LRP-1). The lack of LDL receptors (LDLR) enhances amyloid deposition in the brain while LDLR overexpression increases the rate of Aβ entering the hepatic system. It’s important to consider the effects of organ failure on the development of AD. There are four main factors which contribute to clearance from the body. Blood flow, transport across the blood brain barrier, uptake into the liver, and elimination from the body through bile excretion all play an important role in the clearance of bioaccumulated toxic Aβ and Tau AD inducing proteins.

Keywords: Tau; Beta Amyloid (Aβ); Low-Density Lipoprotein Receptor-Related Peptide 1 (LRP-1); Blood Brain Barrier; Liver; Alzheimer’s Disease (AD)

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