Neuronal expression of STM2 mRNA in human brain is reduced in Alzheimer's disease.
Mutations in the STM2 gene cause familial Alzheimer's disease (AD) in Volga Germans. To understand the function of this protein and how mutations lead to AD, it is important to determine which cell types in the brain express this gene. In situ hybridization histochemistry indicates that STM2 expression in the human brain is widespread and is primarily neuronal. In addition, STM2 mRNA is expressed in a cell line with neuronal origins. Quantification of the level of expression of the STM2 message in the basal forebrain, frontal cortex, and hippocampus reveals a significant decrease in AD-affected subjects compared to normal age-matched controls. These data suggest that downregulation of neuronal STM2 gene expression may be involved in the progression of AD.
McMillan
P J
PJ
Department of Pharmacology, University of Washington, Seattle 98195, USA.
Leverenz
J B
JB
Poorkaj
P
P
Schellenberg
G D
GD
Dorsa
D M
DM
D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D002460:Cell Line; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male; D008565:Membrane Proteins / Q000096:biosynthesis* / Q000235:genetics; D008875:Middle Aged; D053766:Presenilin-2; D012333:RNA, Messenger / Q000096:biosynthesis*
D008565:Membrane Proteins; C508861:PSEN2 protein, human; D053766:Presenilin-2; C095101:Psen2 protein, mouse; D012333:RNA, Messenger