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PMID: 15339642 Published · ppublish English Journal Article Review

Clearance of Alzheimer's Abeta peptide: the many roads to perdition.

Neuron ·Vol. 43 ·No. 5 ·2004-09-02 ·Pages 605-8

Tanzi RE, Moir RD, Wagner SL

Abstract

The amyloid hypothesis of Alzheimer's disease (AD) maintains that the accumulation of the amyloid beta protein (Abeta) is a critical event in disease pathogenesis. A great deal of both academic and commercial research has focused on the mechanisms by which Abeta is generated. However, investigations into the mechanisms underlying Abeta clearance have blossomed over the last several years. This minireview will summarize pathways involved in the removal of cerebral Abeta, including enzymatic degradation and receptor-mediated efflux out of the brain.

MeSH Terms
Alzheimer Disease/metabolism,physiopathology Amyloid beta-Peptides/metabolism Animals Blood-Brain Barrier Brain/metabolism,pathology,physiopathology Humans Insulysin/metabolism Low Density Lipoprotein Receptor-Related Protein-1/metabolism Metabolic Clearance Rate/drug effects,physiology Neprilysin/metabolism Neurons/metabolism,pathology
Chemicals
Amyloid beta-Peptides Low Density Lipoprotein Receptor-Related Protein-1 Neprilysin Insulysin
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Tanzi R E
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Charlestown 02129, USA. tanzi@helix.mgh.harvard.edu
Moir R D
Wagner S L
Article Info
Journal
Neuron
Abbr.
Neuron
ISSN
0896-6273
Published
2004-09-02
Pages
605-8
Language
English
Region
United States
NLM ID
8809320
Subset
IM
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