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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2009-8-18
pubmed:abstractText
Anomalies in glutamate homeostasis may contribute to the pathological processes involved in Alzheimer's disease (AD). Glutamate released from neurons or glial cells is normally rapidly cleared by glutamate transporters, most of which are expressed at the protein level by glial cells. However, in some patho-physiological situations, expression of glutamate transporters that are normally considered to be glial types, appears to be evoked in populations of distressed neurons. This study analysed the expression of exon-skipping forms of the three predominant excitatory amino acid (glutamate) transporters (EAATs1-3) in brains afflicted with AD. We demonstrate by immunocytochemistry in temporal cortex, the expression of these proteins particularly in limited subsets of neurons, some of which appeared to be dys-morphic. Whilst the neuronal expression of the "glial" glutamate transporters EAAT1 and EAAT2 is frequently considered to represent the abnormal and ectopic expression of such transporters, we suggest this may be a misinterpretation, since neurons such as cortical pyramidal cells normally express abundant mRNA for these EAATs (but little if any EAAT protein expression). We hypothesize instead that distressed neurons in the AD brain can turn on the translation of pre-existent mRNA pools, or suppress the degradation of alternately spliced glutamate transporter protein, leading to the "unmasking" of, rather than evoked expression of "glial" glutamate transporters in stressed neurons.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1573-6903
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1748-57
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Neuronal expression of splice variants of "glial" glutamate transporters in brains afflicted by Alzheimer's disease: unmasking an intrinsic neuronal property.
pubmed:affiliation
UQ Centre for Clinical Research and Perinatal Research Centre, Royal Brisbane and Womens Hospital, The University of Queensland, Building 71/918 Herston, Brisbane, QLD 4029, Australia. d.pow@uq.edu.au
pubmed:publicationType
Journal Article, Comparative Study