Abstract:
:Presenilin1 (PSEN1) 1143T and G384A mutations give rise to severe early-onset Alzheimer's disease in two extensively studied Belgian families. In the present study, we examined the effect of PSEN1 1143T and G384A mutations on tau phosphorylation in human SH-SY5Y and mouse Neuro-2a neuroblastoma cell lines that were transiently transfected with wild type (WT) or mutant PSEN1. With a phosphorylation independent antibody, no alteration in the electrophoretic mobility of tau was observed between wild type and mutant PSEN1 transfectants. Also, densitometric analysis of Tau1 immunoreactivity, characteristic of unphosphorylated tau, demonstrated no significant differences between WT and mutant PSEN1 transfectants. Our data suggest that in the cellular models we used, transient overexpression of 1143T and G384A mutant PSEN1 does not lead to increased tau phosphorylation.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Julliams A,Vanderhoeven I,Kuhn S,Van Broeckhoven C,De Jonghe Cdoi
10.1016/s0304-3940(99)00402-4keywords:
subject
Has Abstractpub_date
1999-07-09 00:00:00pages
83-6issue
2eissn
0304-3940issn
1872-7972pii
S0304394099004024journal_volume
269pub_type
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