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