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Abstract #1069

in vivo Axonal Transport Deficits in a Mouse Model of Frontotemporal Dementia

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.

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