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Adams SJ, Crook RJ, Deture M, Randle SJ, Innes AE, Yu XZ, Lin WL, Dugger BN, McBride M, Hutton M, Dickson DW, McGowan E.
Overexpression of wild-type murine tau results in progressive tauopathy and neurodegeneration. Am J Pathol.
2009 Oct;175(4):1598-609.
PubMed Abstract
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Comments on Paper and Primary News |
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Comment by: Takaomi Saido, ARF Advisor
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Submitted 5 September 2009
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Posted 7 September 2009
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 I recommend this paper
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Comment by: Anne Fagan, ARF Advisor
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Submitted 7 September 2009
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Posted 7 September 2009
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I recommend this paper
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Comment by: Richard C. Mohs, ARF Advisor (Disclosure)
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Submitted 8 September 2009
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Posted 9 September 2009
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I recommend this paper
Conditions under which an abnormality in tau processing could lead to neuronal degeneration are of great interest because of their potential implications for the role of tau in human neurodegenerative disease. This paper describes one set of conditions in which tau abnormalities appear to lead directly to neuronal degeneration.  View all comments by Richard C. Mohs |
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Comment by: Jurgen Goetz, ARF Advisor
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Submitted 9 September 2009
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Posted 10 September 2009
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I recommend this paper
This is a nice model with a tauopathy in the absence, apparently, of tau filament formation. This complements the previously generated BAC human tau transgenic mice by Peter Davies and colleagues. Following their line of investigation, it would be interesting to determine whether crossing a conventional human tau transgenic strain with this new BAC murine tau transgenic model causes a more pronounced or an ameliorated phenotype. View all comments by Jurgen Goetz |
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Comments on Related Papers |
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Related Paper: Age-dependent impairment of cognitive and synaptic function in the htau mouse model of tau pathology.
Comment by: Grace (Beth) Stutzmann
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Submitted 7 September 2009
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Posted 7 September 2009
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I recommend this paper
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Related Paper: Age-dependent impairment of cognitive and synaptic function in the htau mouse model of tau pathology.
Comment by: Nancy B. Emerson Lombardo
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Submitted 7 September 2009
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Posted 9 September 2009
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I recommend this paper
Terrific paper. It helps explain what is happening with tau pathology earlier in the process.
If the early tau pathology is reversible, with neurons still living but impaired, one wonders, What are our treatment options? I am particular curious, of course, about possible nutritional approaches.
References:
Emerson Lombardo, NB, Volicer L, Martin A, Wu B. Zhang XW. (2006) Memory preservation diet™ ©2005 to Reduce Risk and Slow Progression of Alzheimer's Disease (AD). In Vellas B, Grundman M, Feldman H, Fitten LJ, Winblad B, editors, Research and Practice in Alzheimer's Disease and Cognitive Decline, vol 9: 138-59.
Emerson Lombardo NB. Martin A. Volicer L. Mandell A. Wen Zhang X. (2006) Comprehensive whole foods diet to reduce risk and slow progression of Alzheimer’s disease. J Nutri Health & Aging 10(3) 211.
Otsuka M, Sato T, Ueki A. (2004) The effect of nutritional intervention on cognitive function in patients with AD J Nutri Health & Aging 8 (5): 428.
View all comments by Nancy B. Emerson Lombardo |
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Related Paper: Age-dependent impairment of cognitive and synaptic function in the htau mouse model of tau pathology.
Comment by: Jurgen Goetz, ARF Advisor
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Submitted 9 September 2009
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Posted 10 September 2009
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I recommend this paper
This is a very carefully performed behavioral and electrophysiological study of an established tau mouse model. AD is a synapse failure. View all comments by Jurgen Goetz |
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REAGENTS/MATERIAL:
The following antibodies were used in this paper:
monoclonal mouse anti-total tau (Tau 5) (Neomarkers, Freemont, CA);
monoclonal mouse anti-phospho-tau S202 (CP13) (provided by Dr. P. Davies, Albert Einstein College of Medicine, Bronx, NY);
monoclonal mouse anti-phospho-tau S396/S404 (PHF1) (provided by Dr. P. Davies, Albert Einstein College of Medicine, Bronx, NY);
monoclonal mouse anti-phospho-tau S202/T205 (AT8) (Pierce Endogen, Rockford, IL);
monoclonal mouse
glyceraldehyde-3-phosphate dehydrogenase (Biodesign International, Kennebunkport, ME);
rabbit anti-GFAP (BioGenex, San Ramon, CA);
polyclonal anti-mouse tau (MS06) (provided by Dr. A. Takashima, RIKEN Brain Science Institute, Wako City, Japan);
goat anti-carbonic anhydrase II (CAII) (provided by Dr. M. S. Ghandour), shown to specifically label oligodendrocytes;
monoclonal mouse anti-neuron-specific nuclear protein (NeuN) (Chemicon International, Billerica, MA)
and anti-tau (WKS44) raised against a tau polypeptide corresponding to amino acid residues 162 to 178, that recognizes a nonphosphorylated tau epitope (provided by Dr. S-H. Yen, Mayo Clinic, Jacksonville, FL)
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