Linked Life Data

9686307

Source:http://linkedlifedata.com/resource/pubmed/id/9686307

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1998-10-22
pubmed:abstractText
Alzheimer's disease (AD) is an archetype of a class of diseases characterized by abnormal protein deposition. In each case, deposition manifests itself in the form of amyloid deposits composed of fibrils of otherwise normal, soluble proteins or peptides. An ever-increasing body of genetic, physiologic, and biochemical data supports the hypothesis that fibrillogenesis of the amyloid beta-protein is a seminal event in Alzheimer's disease. Inhibiting A beta fibrillogenesis is thus an important strategy for AD therapy. However, before this strategy can be implemented, a mechanistic understanding of the fibrillogenesis process must be achieved and appropriate steps selected as therapeutic targets. Following a brief introduction to AD, I review here the current state of knowledge of A beta fibrillogenesis. Special emphasis is placed on the morphologic, structural, and kinetic aspects of this complex process.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1350-6129
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
121-42
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Structural and kinetic features of amyloid beta-protein fibrillogenesis.
pubmed:affiliation
Department of Neurology (Neuroscience), Harvard Medical School Boston, MA, USA. teplow@cnd.bwh.harvard.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't