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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