β ‐Amyloid Degradation and Alzheimer′s Disease

Abstract

Extensive β ‐amyloid (A β ) deposits in brain parenchyma in the form of senile plaques and in blood vessels in the form of amyloid angiopathy are pathological hallmarks of Alzheimer′s disease (AD). The mechanisms underlying A β deposition remain unclear. Major efforts have focused on A β production, but there is little to suggest that increased production of A β plays a role in A β deposition, except for rare familial forms of AD. Thus, other mechanisms must be involved in the accumulation of A β in AD. Recent data shows that impaired clearance may play an important role in A β accumulation in the pathogenesis of AD. This review focuses on our current knowledge of A β ‐degrading enzymes, including neprilysin (NEP), endothelin‐converting enzyme (ECE), insulin‐degrading enzyme (IDE), angiotensin‐converting enzyme (ACE), and the plasmin/uPA/tPA system as they relate to amyloid deposition in AD.

Cited by papers we hold 8

• Novel Approaches for the Treatment of Alzheimer’s and Parkinson’s Disease · 2019
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• Insulin Resistance as a Link between Amyloid-Beta and Tau Pathologies in Alzheimer’s Disease · 2017
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• CALCIUM-SENSING RECEPTORS OF HUMAN NEURAL CELLS PLAY CRUCIAL ROLES IN ALZHEIMER’S DISEASE · 2016
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• Choroid plexus dysfunction impairs beta-amyloid clearance in a triple transgenic mouse model of Alzheimer’s disease · 2015
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• Truncated and modified amyloid-beta species · 2014
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• Neprilysin and Aβ Clearance: Impact of the APP Intracellular Domain in NEP Regulation and Implications in Alzheimer’s Disease · 2013
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• BACE1 is at the crossroad of a toxic vicious cycle involving cellular stress and β-amyloid production in Alzheimer’s disease · 2012
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• Disorder-specific effects of polymorphisms at opposing ends of the <it>Insulin Degrading Enzyme </it>gene · 2011
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