Linked Life Data

15094079

Source:http://linkedlifedata.com/resource/pubmed/id/15094079

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2004-4-19
pubmed:abstractText
Cellular and molecular processes leading to abnormal accumulation of beta amyloid in the brain are slowly being uncovered. A potential involvement of insulin and insulin-like growth factor I (IGF-I) in this plausible pathogenic process in Alzheimer's disease has recently been proposed. Evidence favoring this idea stems from the ability of both hormones to stimulate beta amyloid release from neurons as well as by the stimulatory effect that IGF-I exerts on brain amyloid clearance. In addition, insulin and IGF-I levels are altered in Alzheimer's patients and, probably in close association to these changes, cell sensitivity towards insulin--and possibly also IGF-I--is decreased in these patients. We now review evidence that disturbed insulin/IGF-I signaling to brain cells, initiated at the level of the blood-brain barriers is probably instrumental in development of brain amyloidosis. Furthermore, insulin and IGF-I are potent neuroprotective factors and can regulate levels of phosphorylated tau, a major component of neurofibrillary tangles found in Alzheimer's brains. Therefore, a decrease in trophic support to neurons together with increased tau phosphorylation will follow loss of sensitivity towards insulin and IGF-I. Altogether, this supports the notion that a single pathogenic event, i.e., brain resistance to insulin/IGF-I, accounts for neuronal atrophy/death, tangle formation and brain amyloidosis typical of Alzheimer's pathology.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
19
pubmed:volume
490
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
127-33
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
The role of insulin and insulin-like growth factor I in the molecular and cellular mechanisms underlying the pathology of Alzheimer's disease.
pubmed:affiliation
Laboratory of Neuroendocrinology, Cajal Institute, CSIC, Avenida Doctor Arce 37, Madrid ES 28002, Spain.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't