Physical exercise mitigates behavioral impairments in a rat model of sporadic Alzheimer's disease.

Physical exercise has proven to be beneficial to mitigate several deleterious effects associated with neurodegenerative diseases, including Alzheimer's Disease (AD). Here, we investigated the role of long-term exercise as a preventive and therapeutic tool against AD cognitive and behavioral impairments using a sporadic AD-like rat model, established through the administration of streptozotocin (STZ) inside both cerebral ventricles (icv). Six-weeks-old Wistar male rats (56) were divided into groups (either saline or STZ): sedentary (Sed), voluntary physical activity (VPA), VPA + endurance treadmill training (VPA + ET) and VPA + ET only after the injection (VPA + ET-post). Surgeries occurred at 16wks and the animals were sacrificed at 28 wks. VPA, VPA + ET, and VPA + ET-post had continuous access to the running wheels during the entire experimental protocol. VPA + ET (entire protocol) and VPA + ET-post (only after surgical procedure) ran 60 min/d, 25 m/min, 5d/wk in a treadmill. Both ET regimens led to significant improvements in the compromised spatial learning and long-term memory of STZ-infused animals that were not observed neither in the saline Sed nor in VPA STZ groups. General activity patterns and exploration habits were also ameliorated with chronic-exercise in STZ treated animals, while freezing patterns were decreased in these groups. these results were further. Positive alterations were seen in mitochondrial oxygen consumption endpoints (synaptosomal and non-synaptosomal brain mitochondria) that might underlie the neurobehavioral improvements observed. Data suggest that VPA alone was not able to counteract the AD-related deleterious consequences, although when accompanied by endurance training (either lifelong or later-life) may be able to prevent and reverse cognitive and phenotypic impairments associated with AD.