Linked Life Data

16457902

Source:http://linkedlifedata.com/resource/pubmed/id/16457902

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-3-13
pubmed:abstractText
The conversion of what has been interpreted as "normal brain aging" to Alzheimer's disease (AD) via a transition state, i.e. mild cognitive impairment, appears to be a continuous process caused primarily by aging-dependent accumulation of amyloid beta peptide (Abeta) in the brain. This notion give us a hope that, by manipulating the Abeta levels in the brain, we may be able not only to prevent and cure the disease but also to partially control some very significant aspects of brain aging. Abeta is constantly produced from its precursor and immediately catabolized under normal conditions, whereas dysmetabolism of Abeta seems to lead to pathological deposition upon aging. We have focused our attention on elucidation of the unresolved mechanism of Abeta catabolism in the brain. In this review, we describe a new approach to prevent AD development by reducing Abeta burdens in aging brains through up-regulation the catabolic mechanism involving neprilysin that can degrade both monomeric and oligomeric forms of Abeta. The strategy of combining presymptomatic diagnosis with preventive medicine seems to be the most pragmatic in both medical and socio-economical terms. We also introduce a novel non-invasive amyloid imaging approach using a high-power magnetic resonance imaging (MRI) for the presymptomatic diagnosis of AD.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0168-0102
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
235-53
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Metabolism of amyloid beta peptide and pathogenesis of Alzheimer's disease. Towards presymptomatic diagnosis, prevention and therapy.
pubmed:affiliation
Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako-shi, Saitama, Japan. saido@brain.riken.jp
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't