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Abstract #2226

Nano-antioxidants improve axonal transport deficits in a mouse model of Alzheimers disease

Kelly Ann Moore 1 , Errol Loc Samuel 2 , James Tour 2 , and Robia G Pautler 1

1 Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas, United States, 2 Department of Chemistry, Rice University, Houston, Texas, United States

Studies have shown in multiple models of Alzheimers disease that deficits in fast axonal transport develop before amyloid-beta plaque and tau deposition, with oxidative stress being implicated in the process. Using an APP/PSEN1 model of Alzheimers disease we demonstrate via manganese enhanced MRI a deficit in the axonal transport of this model. Additionally we show that these deficits can be reversed with the administration of nano-antioxidant PEG-ylated-hydrophilic carbon clusters.

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