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Abstract Details

Abstract Title

Effects of resistance exercise program in mice with Alzheimer's Disease

Abstract Theme

Neuroscience and sport

Type Presentation

Poster

Abstract Authors

Presenter Matheus Libarino Santos - Federal University of São Paulo (Physiology) - BR
Giovana Pellizzon - Federal University of São Paulo (Physiology) - BR
Christiane Gimenes - Federal University of São Paulo (Physiology) - BR
Caio Souza - Federal University of São Paulo (Physiology) - BR
Juliana Trevizo - Federal University of São Paulo (Physiology) - BR
Eduardo A. da Silva - Federal University of São Paulo (Physiology) - BR
Alexandre J. Lima - State University (Health Science) - BR
Jansen Fernandes - Federal University of São Paulo (Physiology) - BR
Sergio Gomes da Silva - University of Mogi das Cruzes (Physiology) - BR
Ricardo Mario Arida - Federal University of São Paulo (Physiology) - BR
Beatriz M. Longo - Federal University of São Paulo (Physiology) - BR

Presentation Details

Poster Exhibition Site (Local): Orange - 1        Date: 1 September        Time: 8am to 7pm        Presenter: MATHEUS SANTOS

Abstract Resume

Background: Alzheimer's disease (AD) is a neurodegenerative disease that mainly affects functions such as cognitive behavior and memory. Considering these cognitive deficits and the
absence of an effective treatment, physical activity has emerged as an alternative treatment to prevent or retard the progression of AD. It has been shown that aerobic exercise is able to increase
neurogenic factors, modulate inflammation and decrease the number of amyloid plaques present in the brain, especially in the cortex and hippocampus. Here, we hypothesized whether a program of
resistance exercise could interfere on the reduction of amyloid plaques and number of neurogenic cells in the cortex and hippocampus. To investigate this idea, we evaluated the effects of a resistance
exercise program in the brain of transgenic mice for AD.

Methods: Double transgenic mice with APPswe/PS1dE9 mutation, with 7-9 months old were used as Alzheimer's disease model, and the respective wild type mice (WT) used as controls. Mice
were divided into four groups: AD with exercise (AD+EX; n =6), control with exercise (WT+EX; n =6), AD without exercise (AD; n =5) and control without exercise (WT; n =5), and the exercise groups were
subjected to resistance exercise of climbing force with overload. Following a maximum load test once a week, each animal was subjected to the resistance exercise protocol consisted of eight climbing
series with a progressively heavier load. Each series contained an average of 8 to 12 climbing movements, 5 days/week, 4 weeks. After the last day of exercise, animals were perfused with
paraformaldehyde (4%), their brains were removed from the skull, frozen and cryostat cut (30µm). The slices were processed for immunohistochemistry for β-amyloid (6E-10) to stain the amyloid plaques
in the cortex and hippocampus, and for doublecortin (DCX) staining neurogenic cells in the hippocampus.

Results: Quantitative analysis of amyloid plaques indicated a significant reduction of β-amyloid in both cortex (p = 0.0031) and hippocampus (p = 0.0285) of the AD+EX group; the DCX
positive cells counted in the hippocampus indicated a reduction in neurogenesis in both AD and AD+EX groups (p < 0.005), although no significant difference was detected between the groups subjected to
physical activity.

Conclusions: Our data indicate that the resistance exercise program is able to reduce the number of amyloid plaques in both hippocampus and cortex, with no direct effects on
neurogenesis. Based on these results, the resistance exercise (in addition to the aerobic exercise) can be proposed as a new candidate in the adjuvant treatment of AD.

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