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P3‐004: Voluntary exercise in THY‐Tau22 mice prevents tau pathology and its consequences
Author(s) -
BuéeScherrer Valérie,
Burnouf Sylvie,
Belarbi Karim,
FernandezGomez FranciscoJose,
Laurent Cyril,
Troquier Laetitia,
Leboucher Antoine,
Caillierez Raphaëlle,
Sergeant Nicolas,
Hamdane Malika,
Buée Luc,
Blum David
Publication year - 2011
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2011.05.1443
Subject(s) - neuroscience , tau pathology , dementia , psychology , cognition , disease , cognitive decline , hippocampal formation , entorhinal cortex , tau protein , hippocampus , medicine , alzheimer's disease , pathology
pressing the responder transgene are maintained on a FVB/NCrl strain. All bigenic progeny will be on a strain background that is 50% FVB and 50% 129S. To address the effect of strain background on pathology progression in this model, we have created a B6/rTg4510 mouse line in which the same responder mice on the FVB/NCrl background are now bred with C57BL/6J mice expressing the activator transgene to create bigenic offspring that are now 50% FVB and 50% B6. To determine if the introduction of the B6 background would delay the pathological progression, we have harvested cohorts of B6/rTg4510 mice at 5.5M, 6.5M and 10.5M of age. Tau pathology will be assessed by biochemical and immunohistochemical analysis. To assess effects on cognition, we have also behaviorally tested the 6.5M and 10.5M cohorts with the Morris water maze. Results: Initial biochemical analysis of soluble and sarkosyl-insoluble tau by western blot analysis shows that B6/rTg4510 mice do not have a delay in the progression of tau pathology as compared to the original rTg4510 line. Interestingly though, the B6/rTg4510 females have a trending increase in 64kd tau as compared to males of their own line and males and females of the original rTg4510 line. Further analysis is ongoing to determine the nature and significance of the initial differences detected. Behavioral data supports the initial biochemical analysis in that both lines are cognitively impaired and do not significantly differ in this impairment from one another. Immunohistochemical analysis is ongoing and will be complete by March 15. At the time of the conference, full behavioral, biochemical and immunohistochemical analysis will be presented. Conclusions: Unlike the previous report of a delay in tauopathy progression in the JNPL3 transgenic mouse line with the introduction of the C57BL/ 6J background strain, we do not observe the same changes in the rTg4510 mouse model as assessed by behavior and preliminary biochemical analysis. Immunohistochemical analysis is ongoing and a full assessment will be presented.