Linked Life Data

15094078

Source:http://linkedlifedata.com/resource/pubmed/id/15094078

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
Nosologically, Alzheimer disease is not a single disorder in spite of a common clinical phenotype. Etiologically, two different types or even more exist. (1) In a minority of about 5% or less of all cases, Alzheimer disease is due to mutations of three genes, resulting in the permanent generation of betaA4. (2) The great majority (95% or more) of cases of Alzheimer disease are sporadic in origin, with old age as main risk factor, supporting the view that susceptibility genes and aging contribute to age-related sporadic Alzheimer disease. However, disturbances in the neuronal insulin signal transduction pathway may be of central pathophysiological significance. In early-onset familial Alzheimer disease, the inhibition of neuronal insulin receptor function may be due to competitive binding of amyloid beta (Abeta) to the insulin receptor. In late-onset sporadic Alzheimer disease, the neuronal insulin receptor may be desensitized by inhibition of receptor function at different sites by noradrenaline and/or cortisol, the levels of which both increase with increasing age. The consequences of the inhibition of neuronal insulin signal transduction may be largely identical to those of disturbances of oxidative energy metabolism and related metabolism, and of hyperphosphorylation of tau-protein. As far as the metabolism of amyloid precursor protein (APP) in late-onset sporadic Alzheimer disease is concerned, neuronal insulin receptor dysfunction may result in the intracellular accumulation of Abeta and in subsequent cellular damage. In this context, the desensitization of the neuronal insulin receptor in late-onset sporadic Alzheimer disease is different from that occurring in normal aging and early-onset familial Alzheimer disease. In late-onset sporadic Alzheimer disease changes in the brain are similar to those caused by non-insulin-dependent diabetes mellitus.
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
115-25
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Glucose metabolism and insulin receptor signal transduction in Alzheimer disease.
pubmed:affiliation
Department of Pathology, University of Heidelberg, Im Neuenheimer Feld 220/221, 69120 Heidelberg, Germany. siegfried_hoyer@med.uni-heidelberg.de
pubmed:publicationType
Journal Article, Review