Clearance of Alzheimer's Abeta peptide: the many roads to perdition.
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.
Tanzi
R E
RE
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
RD
Wagner
S L
SL
D000544:Alzheimer Disease / Q000378:metabolism* / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D001812:Blood-Brain Barrier; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007339:Insulysin / Q000378:metabolism; D026503:Low Density Lipoprotein Receptor-Related Protein-1 / Q000378:metabolism; D008657:Metabolic Clearance Rate / Q000187:drug effects / Q000502:physiology; D015260:Neprilysin / Q000378:metabolism; D009474:Neurons / Q000378:metabolism* / Q000473:pathology
D016229:Amyloid beta-Peptides; D026503:Low Density Lipoprotein Receptor-Related Protein-1; D015260:Neprilysin; D007339:Insulysin