Clearing amyloid through the blood-brain barrier

J Neurochem. 2004 May;89(4):807-11. doi: 10.1111/j.1471-4159.2004.02385.x.


According to the amyloid hypothesis, accumulation of amyloid beta-peptide (A beta) in the brain is the primary pathogenic event in Alzheimer's disease (AD). Recent evidence indicates that A beta within the intravascular space is linked to A beta deposited in the brain suggesting that transport of A beta between the brain, blood and cerebrospinal fluid, and across the blood-brain barrier, regulates brain A beta. Thus, understanding A beta exchanges between brain and blood, and vice versa, and developing transport-based systemic A beta-lowering strategies may provide new important insights into pathogenesis and therapeutic control of AD.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / therapy
  • Amyloid / metabolism*
  • Amyloid beta-Peptides / metabolism
  • Animals
  • Blood-Brain Barrier / metabolism*
  • Brain / blood supply
  • Brain / metabolism
  • Humans
  • LDL-Receptor Related Proteins / metabolism
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic / metabolism


  • Amyloid
  • Amyloid beta-Peptides
  • LDL-Receptor Related Proteins
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic