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Therapeutic Potential of Direct Clearance of the Amyloid-β in Alzheimer’s Disease

Massachusetts College of Pharmacy and Health Science University, Boston, MA 02115, USA
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Author to whom correspondence should be addressed.
Brain Sci. 2020, 10(2), 93; https://doi.org/10.3390/brainsci10020093
Received: 23 January 2020 / Revised: 5 February 2020 / Accepted: 5 February 2020 / Published: 10 February 2020
(This article belongs to the Section Molecular and Cellular Neuroscience)
Alzheimer’s disease (AD) is characterized by deposition and accumulation of amyloid-β (Aβ) and its corresponding plaques within the brain. Although much debate exists whether these plaques are the cause or the effect of AD, the accumulation of Aβ is linked with the imbalance between the production and clearance of Aβ. The receptor for advanced glycation endproducts (RAGE) facilitates entry of free Aβ from the peripheral stream. Conversely, lipoprotein receptor-related protein 1 (LRP1), located in the abluminal side at the blood–brain barrier mediates the efflux of Aβ. Research on altering the rates of clearance of A by targeting these two pathways has been extensively study. Additionally, a cerebrospinal fluid (CSF) circulation assistant device has also been evaluated as an approach to increase solute concentration in the CSF via mechanical drainage, to allow for removal of Aβ from the brain. Herein, we provide a brief review of these approaches that are designed to re-establish a homeostatic Aβ balance in the brain.
Keywords: Alzheimer’s disease; amyloid-β; lipoprotein receptor-related protein 1; receptor for advanced glycation endproducts; cerebrospinal fluid Alzheimer’s disease; amyloid-β; lipoprotein receptor-related protein 1; receptor for advanced glycation endproducts; cerebrospinal fluid
MDPI and ACS Style

Kim, D.E.; Priefer, R. Therapeutic Potential of Direct Clearance of the Amyloid-β in Alzheimer’s Disease. Brain Sci. 2020, 10, 93.

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