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PURPOSE This study is to investigate the effects of treadmill exercise on iron accumulation and microglial cell activity in the cerebral cortex of APP-C105 transgenic Alzheimer’s mice. METHODS The transgenic mice and their comparative non-transgenic mice at 24 months of age were divided into 3 groups: NTC (Non-Tg-Con, n=7), TC (Tg-Con, n=7), TE (Tg-Exe, n=7). TE group ran on the treadmill (30 min/day, 5 day/week) for 8 weeks. RESULTS The results show that treadmill exercise significantly improved spatial memory and cognitive function in TE group compared with TC group in Morris water-maze test and Passive avoidance test. In addition, TE group with treadmill exercise showed to decrease significantly in the accumulation level of iron, amyloid-beta protein, activated-microglia factor and pro-inflammation factor in comparison with TC group. anti-inflammation factor TE group was significantly increased than TC group. CONCLUSIONS These results suggest that treadmill exercise has positive effects on cognitive function, iron accumulation level of iron and activated-microglia factor and it can act as a key role for clinical strategy in AD.

Alzheimer's disease (AD) is a neurodegenerative disorder associated with extracellular plaques, composed of amyloid-beta (Aβ), in the brain. Although the precise mechanism underlying the neurotoxicity of Aβ has not been established, Aβ accumulation is the primary event in a cascade of events that lead to neurofibrillary degeneration and dementia. In particular, the Aβ burden, as assessed by neuroimaging, has proved to be an excellent predictive biomarker. Positron emission tomography, using ligands such as 11C-labeled Pittsburgh Compound B or 18F-labeled tracers, such as 18F-florbetaben, 18F-florbetapir, and 18F-flutemetamol, which bind to Aβ deposits in the brain, has been a valuable technique for visualizing and quantifying the deposition of Aβ throughout the brain in living subjects. Aβ imaging has very high sensitivity for detecting AD pathology. In addition, it can predict the progression from mild cognitive impairment to AD, and contribute to the development of disease-specific therapies.