Tau isoform expression in frontotemporal dementia without tau deposition.
In many cases of sporadic frontotemporal dementia (FTD) and in FTD caused by tau mutations (FTDP-17) there is disruption of the normal splicing of tau leading to the aberrant expression of tau isoforms and neurodegeneration. This suggests a central role for tau in the pathogenesis of FTD. However, more than half the cases of sporadic FTD show no tau deposition. We question whether altered expression is also involved in the pathogenesis of tau-negative FTD. Real-time polymerase chain reaction was used to investigate tau isoform expression in tau-negative FTD and age-matched controls. There were no differences in total tau mRNA or 4R versus 3R isoform expression. Our study suggests that perturbed tau mRNA expression is unlikely to be involved in the pathogenesis of tau-negative FTD.
Sutherland
Greg T
GT
Centre for Education and Research on Ageing, The University of Sydney, Sydney, 2006, New South Wales, Australia.
Nowak
Greg
G
Halliday
Glenda M
GM
Kril
Jillian J
JJ
D000368:Aged; D000369:Aged, 80 and over; D003704:Dementia / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000378:metabolism; D006801:Humans; D007536:Isomerism; D008297:Male; D008875:Middle Aged; D009778:Occipital Lobe / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016875:tau Proteins / Q000096:biosynthesis* / Q000737:chemistry / Q000378:metabolism*
D012333:RNA, Messenger; D016875:tau Proteins; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases