Alzheimer's disease (AD) is associated with cognitive deficits and behavioral disorders such as anxiety and depression. Recent clinical and experimental studies have demonstrated that swimming exercise could be a potential therapy for cognitive and behavioral disorders. The prevalence of anxiety and depression is increasing among patients with AD; hence, further studies are needed to develop therapies for these behavioral abnormalities. The purpose of this study was to evaluate the effects of swimming exercise on memory impairment, anxiety, and depression-like behaviors in a mouse model of sporadic Alzheimer-like disease. Eight days after AD induction by streptozotocin (STZ), mice were subjected to the swimming exercise for four weeks. To assess cognitive functions, anxiety- and depression-related behaviors in animals, Y-maze, novel object recognition, open field, zero maze, sucrose preference, and forced swim tests were used. To understand the possible mechanisms, amyloid-β (Aβ)-42, brain-derived neurotrophic factor (BDNF), glutamate, malondialdehyde (MDA), tumor-necrosis-factor (TNF)-α, and interleukin (IL)-6 levels were measured in the hippocampus. The results of this study indicate that STZ administration impaired cognitive functions, increased anxiety- and depression-related behaviors, and elevated Aβ-42, glutamate, MDA, TNF-α, and IL-6 levels in the hippocampus of mice. In contrast, swimming exercise significantly reversed these neurobehavioral disorders, increased BDNF, and decreased both glutamate and TNF-α in the hippocampus of STZ-treated mice. Overall, these findings provide some support for the idea that swimming exercise might be associated with reduced neurobehavioral disorders in patients with Alzheimer's disease. However, further clinical studies on this topic are required to confirm and validate these findings.
Physiology and Behavior, Volume 223, 1 September 2020,