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

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

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

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