Linked Life Data

20833262

Source:http://linkedlifedata.com/resource/pubmed/id/20833262

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2010-11-8
pubmed:abstractText
The accumulation of amyloid-beta (A?) peptides is believed to be a central contributor to the neurodegeneration typically seen in Alzheimer's disease (AD) brain. A? extracted from AD brains invariably possesses extensive truncations, yielding peptides of differing N- and C-terminal composition. Whilst A? is often abundant in the brains of cognitively normal elderly people, the brains of AD patients are highly enriched for N-terminally truncated A? bearing the pyroglutamate modification. Pyroglutamate-A? (pE-A?) has a higher propensity for oligomerisation and aggregation than full-length A?, potentially seeding the accumulation of neurotoxic A? oligomers and amyloid deposits. In addition, pE-A? has increased resistance to clearance by peptidases, causing these peptides to persist in biological fluids and tissues. The extensive deposition of pE-A? in human AD brain is under-represented in many transgenic mouse models of AD, reflecting major differences in the production and processing of A? peptides in these models compared to the human disease state.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1878-5875
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1915-8
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Pyroglutamate-A?: Role in the natural history of Alzheimer's disease.
pubmed:affiliation
The Mental Health Research Institute, Parkville, VIC, Australia.
pubmed:publicationType
Journal Article, Review