Linked Life Data

7504355

Source:http://linkedlifedata.com/resource/pubmed/id/7504355

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1993-12-29
pubmed:abstractText
The progressive deposition of the beta-amyloid peptide in the brain and its microvasculature is an invariant feature of Alzheimer's disease that appears to precede the onset of dementia by many years. It had been assumed that the proteolytic release of beta-amyloid peptide from the transmembrane region of its large precursor protein was an aberrant event, requiring prior membrane injury. However, it has recently been shown that beta-amyloid peptide is continuously secreted from healthy neural and non-neural cells in culture and circulates in human CSF and blood. The finding that beta-amyloid peptide is a normal, soluble product of cellular metabolism has led to many dynamic studies of its formation and clearance in health and in genetic forms of Alzheimer's disease, and should facilitate the design of amyloid-inhibiting therapeutics.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0166-2236
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
403-9
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Physiological production of the beta-amyloid protein and the mechanism of Alzheimer's disease.
pubmed:affiliation
Center for Neurologic Diseases, Harvard Medical School, Boston, MA 02115.
pubmed:publicationType
Journal Article, Review