Linked Life Data

15751228

Source:http://linkedlifedata.com/resource/pubmed/id/15751228

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-3-8
pubmed:abstractText
Insulin-degrading enzyme (IDE) has been identified as a candidate protease in the clearance of amyloid-delta (Abeta) peptides from the brain. IDE activity and binding to insulin are known to be inhibited by glucocorticoids in vitro. In Alzheimer disease (AD), both a decrease in IDE levels and an increase in peripheral glucocorticoid levels have been documented. Our study investigated the effects of glucocorticoid treatment on IDE expression in vivo in 12 nonhuman primates (Macaca nemestrina). Year-long, high-dose exposure to the glucocorticoid cortisol (hydrocortisone acetate) was associated with reduced IDE protein levels in the inferior frontal cortex and reduced IDE mRNA levels in the dentate gyrus of the hippocampus. We assessed Abeta40 and Abeta42 levels by ELISA in the brain and in plasma, total plaque burden by immunohistochemistry, and relative Abeta1-40 and Abeta1-42 levels in the brain by mass spectrometry. Glucocorticoid treatment increased Abeta42 relative to Abeta40 levels without a change in overall plaque burden within the brain, while Abeta42 levels were decreased in plasma. These findings support the notion that glucocorticoids regulate IDE and provide a mechanism whereby increased glucocorticoid levels may contribute to AD pathology.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-3069
pubmed:author
pubmed:issnType
Print
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
139-46
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Effects of chronic glucocorticoid administration on insulin-degrading enzyme and amyloid-beta peptide in the aged macaque.
pubmed:affiliation
Geriatric Research, Education, and Clinical Center, Veteran's Affairs Puget Sound Health Care System, Seattle, Washington 98108, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't