Linked Life Data

17234594

Source:http://linkedlifedata.com/resource/pubmed/id/17234594

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-1-19
pubmed:abstractText
Numerous studies have established a pivotal role for Abeta42 in Alzheimer's disease (AD) pathogenesis. In contrast, although Abeta40 is the predominant form of amyloid beta (Abeta) produced and accumulates to a variable degree in the human AD brain, its role in AD pathogenesis has not been established. It has generally been assumed that an increase in Abeta40 would accelerate amyloid plaque formation in vivo. We have crossed BRI-Abeta40 mice that selectively express high levels of Abeta40 with both Tg2576 (APPswe, K670N+M671L) mice and BRI-Abeta42A mice expressing Abeta42 selectively and analyzed parenchymal and cerebrovascular Abeta deposition in the bitransgenic mice compared with their singly transgenic littermates. In the bitransgenic mice, the increased steady-state levels of Abeta40 decreased Abeta deposition by 60-90%. These results demonstrate that Abeta42 and Abeta40 have opposing effects on amyloid deposition: Abeta42 promotes amyloid deposition but Abeta40 inhibits it. In addition, increasing Abeta40 levels protected BRI-Abeta40/Tg2576 mice from the premature-death phenotype observed in Tg2576 mice. The protective properties of Abeta40 with respect to amyloid deposition suggest that strategies that preferentially target Abeta40 may actually worsen the disease course and that selective increases in Abeta40 levels may actually reduce the risk for development of AD.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
17
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
627-33
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Abeta40 inhibits amyloid deposition in vivo.
pubmed:affiliation
Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, Florida 32224, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural