Faculty Opinions recommendation of Formation of neurofibrillary tangles in P301l tau transgenic mice induced by Abeta 42 fibrils.

Author(s):  
James Goldman
2009 ◽  
Vol 5 (4S_Part_17) ◽  
pp. e29-e29 ◽  
Author(s):  
Frank M. LaFerla ◽  
Hilda Martinez-Coria ◽  
Kim N. Green ◽  
Pradeep K. Banerjee

2010 ◽  
Vol 19 (2) ◽  
pp. 705-719 ◽  
Author(s):  
Karelle Leroy ◽  
Kunie Ando ◽  
Céline Héraud ◽  
Zehra Yilmaz ◽  
Michèle Authelet ◽  
...  

2007 ◽  
Vol 171 (3) ◽  
pp. 976-992 ◽  
Author(s):  
Karelle Leroy ◽  
Alexis Bretteville ◽  
Katharina Schindowski ◽  
Emmanuel Gilissen ◽  
Michèle Authelet ◽  
...  

2000 ◽  
Vol 6 (S2) ◽  
pp. 584-585
Author(s):  
W.-L. Lin ◽  
J. Lewis ◽  
A.R. Corral ◽  
D.W. Dickson ◽  
M. Hutton

Tau is a microtubule-associated protein that promotes polymerization and stabilization of microtubules. It is the major component of fibrillary neuronal and glial inclusions in Alzheimer's disease (AD) and the tauopathies. An autosomal dominant familial tauopathy, frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), has been shown to be caused by pathogenic tau mutations. Neuropathologic features of FTDP-17 are filamentous tau aggregates in neurons and glia. Previous transgenic mice carrying the normal human tau gene developed motor neuron disease and had dystrophic axons, but no neurofibrillary tangles (NFT). In this report we describe ultrastructural features of NFT in transgenic mice carrying a mutant human tau gene. The mice were generated with a tau cDNA containing exon 1, 4, 5, 7, 9, 10, 11-13, intron 13 and exon 14, driven by the mouse prion promoter (MoPrP) and containing the most common FTDP-17 mutation, P301L. The transgenic construct was generated by ligating the P301L tau cDNA with the mouse prion promoter.


2004 ◽  
Vol 25 ◽  
pp. S246
Author(s):  
Cathy A. Andorfer ◽  
Christopher M. Acker ◽  
Yvonee Kress ◽  
Karen Duff ◽  
Peter Davies

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