Abstract #4327
Mitochondrial Catalase Overexpression recovers axonal transport deficits and improves hippocampal long-term potentiation in APP/PS1 mice
Tabassum Majid 1,2 , Caiwei Guo 3 , Tao Ma 4 , Erik Klann 4 , and Robia Pautler 1,2
1
Translational Biology and Molecular
Medicine, Baylor College of Medicine, Houston, Texas,
United States,
2
Molecular
Physiology & Biophysics, Baylor College of Medicine,
Houston, Texas, United States,
3
Department
of Neuroscience, Baylor College of Medicine, Houston,
Texas, United States,
4
New
York University, New York, New York, United States
Antioxidant therapies for Alzheimer's disease (AD) have
been met with limited success. Previous work from our
lab has demonstrated that genetic superoxide dismutase 2
overexpression can ameliorate Alzheimer's pathology in
the Tg2576 mouse model of AD. After establishing the
role of superoxide in the pathogenesis of AD, we sought
to explore the role of catalase overexpression in an
aggressive AD model (APP/PS1). We report improvements in
axonal transport rate as well as significant
improvements in long-term potentiation within the
hippocampus. From our findings, we add evidence to
elucidate the role of specific redox species in AD.
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