Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1990-8-30
pubmed:abstractText
The studies described here provide convincing evidence of glutamatergic deafferentation in Alzheimer's disease. This deafferentation is presumed to represent the biochemical correlate of pyramidal neuron dysfunction in the disorder. In addition, there is a growing consensus of opinion that there is no widespread depletion of glutamate NMDA receptors in Alzheimer's disease. The significance of glutamatergic neurotransmission abnormalities to the pathogenesis and clinical progression of the disease remains to be established.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0300-5127
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
390-2
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Glutamatergic neurotransmission in Alzheimer's disease.
pubmed:affiliation
Department of Biochemistry and Molecular Genetics, St Mary's Hospital Medical School, University of London, U.K.
pubmed:publicationType
Journal Article, Review