Linked Life Data

21330304

Source:http://linkedlifedata.com/resource/pubmed/id/21330304

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-4-14
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1089-4098
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
163-73
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Sink hypothesis and therapeutic strategies for attenuating Abeta levels.
pubmed:affiliation
Laboratory of Neurobiology and State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing, 100871, China. yanzhang@pku.edu.cn
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't