Tabassum Majid1,
2, Yousuf Ali3, Ming-Kuei Jang4, Hui-Chen Lu5,
6, Robia G. Pautler, 27
1Molecular
Physiology and Biophysics, Baylor College of Medicine, Houston, TX, United
States; 2Interdepartmental Program in Translational Biology and Molecular
Medicine, Baylor College of Medicine, Houston, TX, United States; 3Pediatrics-Neurology,
Baylor College of Medicine Cain Foundation Laboratories, Houston, TX, United
States; 4Institute for Applied Cancer Science, The University of
Texas MD Anderson Cancer Center, Houston, TX, United States; 5Department
of Pediatrics, Baylor College of Medicine Cain Foundation Laboratories,
Houston, TX, United States; 6Department of Neuroscience, Baylor
College of Medicine, Houston, TX, United States; 7Department of
Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX,
United States
In vivo axonal transport deficits have been reported prior to plaque pathology in mouse models of Alzheimers disease. However, there are limited in vivo measurements of axonal transport in models of other neurodegenerative diseases such as frontotemporal dementia (FTDP-17). In the r(tta)Tg4510 mouse model, the P301L tau mutation is conditionally expressed throughout the forebrain. In this study, we characterized 10 month old r(tta)Tg4510 mice and found significant deficits in axonal transport in olfactory neurons. This study provides a basis to characterize earlier time points in the r(tta)Tg4510 mouse model in order to investigate therapeutic interventions in this mouse model.