| pubmed-article:21330304 | pubmed:abstractText | Amyloid ? (A?) plaque, comprised mainly by A? peptides, is an important pathology of Alzheimer's brains. Major efforts have been devoted to targeting this neurotoxic A? peptide for discovering disease-modifying treatments for Alzheimer's disease. Inasmuch as A? is found in both the brain and the periphery, it is hypothesized that there is some form of equilibrium for the A? in the brain and the periphery such that A? can be transported across the blood-brain barrier. By modulating the periphery A? levels, it is predicted that the brain A? levels will undergo concomitant changes, forming the basis of the "sink hypothesis" for A? lowering strategies. In this review, the significance and implication of this sink hypothesis as well as how the sink hypothesis may contribute to the recent A?-based drug discovery in AD are discussed. Ultimately, the validity of the sink hypothesis will be resolved when the appropriate A? agents are being tested in the clinic. | lld:pubmed |
