Linked Life Data

18775683

Source:http://linkedlifedata.com/resource/pubmed/id/18775683

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2008-10-22
pubmed:abstractText
Radiologic and neuropsychologic studies suggest that diabetes mellitus causes structural changes in the brain and adversely effects cognitive development. Experimental animal models of type 1 diabetes mellitus (T1DM) have advanced these findings by demonstrating duration-related neuronal and cognitive deficits in T1DM BB/Wor rats. We studied the expression of receptor for advanced glycation end products (RAGE) and neuronal densities in the brains of two patients who died as the result of clinical brain edema(BE)that developed during the treatment of severe diabetic ketoacidosis (DKA). RAGE was markedly and diffusely expressed in blood vessels, neurons, and the choroid plexus and co-localized with glial fibrillary acidic protein (GFAP) in astrocytes. Significant neuronal loss was seen in the hippocampus and frontal cortex. Astrocytosis was present and white matter was atrophied in both cases when compared to age-matched controls. Our data supports that a neuroinflammatory response occurs in the BE associated with DKA, and that even after a relatively short duration of poorly controlled T1DM, the pathogenesis of primary diabetic encephalopathy can be initiated.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1872-6240
pubmed:author
pubmed:issnType
Electronic
pubmed:day
31
pubmed:volume
1238
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
154-62
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Receptor for advanced glycation end products and neuronal deficit in the fatal brain edema of diabetic ketoacidosis.
pubmed:affiliation
Department of Pediatrics, Section of Pediatric Endocrinology, Medical College of Georgia, Augusta, GA 30912, USA. whoffman@mail.mcg.edu
pubmed:publicationType
Journal Article, Case Reports