Source:http://linkedlifedata.com/resource/pubmed/id/12065626
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
2002-6-14
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| pubmed:abstractText |
Amyloid precursor protein (APP) dysfunction is a key aetiologic agent in Alzheimer's disease (AD). The processing of this transmembrane protein generates carboxy terminal fragments (CTFs) upstream of beta-amyloid peptide (Abeta) production. The physiologic significance of APP-CTFs is still poorly understood, as well as the relationship that could link APP dysfunction and tau pathology in familial and non-familial AD (non-FAD). In the present study, we have investigated the quantitative and qualitative changes of APP-CTFs in different brain areas of non-demented and demented patients from a prospective and multidisciplinary study. A significant decrease of the five APP-CTFs was observed, which correlated well with the progression of tau pathology, in most cases with infraclinical AD and AD, either familial or non-FAD. Furthermore, solubility properties and the ratio between the five bands were also modified, both in the Triton-soluble and/or -insoluble fractions. Together, we show here for the first time a modification directly observed on APP-CTFs upstream of Abeta products and its relationship with tau pathology, which could reflect the basic aetiological mechanisms of AD.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
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| pubmed:issn |
0022-3042
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
81
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
663-72
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:12065626-Aged,
pubmed-meshheading:12065626-Aged, 80 and over,
pubmed-meshheading:12065626-Alzheimer Disease,
pubmed-meshheading:12065626-Amyloid beta-Protein Precursor,
pubmed-meshheading:12065626-Blotting, Western,
pubmed-meshheading:12065626-Brain,
pubmed-meshheading:12065626-Brain Chemistry,
pubmed-meshheading:12065626-Disease Progression,
pubmed-meshheading:12065626-Electrophoresis, Gel, Two-Dimensional,
pubmed-meshheading:12065626-Humans,
pubmed-meshheading:12065626-Middle Aged,
pubmed-meshheading:12065626-Peptide Fragments,
pubmed-meshheading:12065626-Phosphorylation,
pubmed-meshheading:12065626-Precipitin Tests,
pubmed-meshheading:12065626-Prospective Studies,
pubmed-meshheading:12065626-Protein Processing, Post-Translational,
pubmed-meshheading:12065626-Solubility,
pubmed-meshheading:12065626-tau Proteins
|
| pubmed:year |
2002
|
| pubmed:articleTitle |
Progressive decrease of amyloid precursor protein carboxy terminal fragments (APP-CTFs), associated with tau pathology stages, in Alzheimer's disease.
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| pubmed:affiliation |
INSERM U422, 1 Place de Verdun, 59045 Lille Cedex, France.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|