Brittany R. Bitner1,2, Taeko Inoue1,
Lingyun Hu1, Chi An Chiang3, Robia G. Pautler1,2
1Molecular Physiology &
Biophysics, Baylor College of Medicine, Houston, TX, United States; 2Translational
Biology & Molecular Medicine, Baylor College of Medicine, Houston, TX,
United States; 3Neuroscience, Baylor College of Medicine
Alzheimers disease (AD) is the most common form of age-related dementia. Previous studies have shown that the overexpression of the mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD) in a mouse model of AD (Tg2576) can reduce pathological findings. To determine whether SOD overexpression in Tg2576 AD mice (SOD/AD) can recover structural changes, we imaged aged SOD/AD mice and their littermates (AD, SOD, and wildtype) using diffusion tensor imaging. We found that AD mice had significant deficits in their fractional anisotropy and apparent diffusion coefficient compared to controls in several brain regions while SOD/AD mice exhibited significant recovery.
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