Abstract
Many studies suggest that regular exercise could reduce memory impairment, the main symptoms of Alzheimer's disease (AD), but the underlying mechanisms has not been elucidated. Inflammation incuded by β-amyloid (Aβ) deposition has been shown to play an critical role in AD pathogenesis. Increasing evidence show that aerobic exercise has anti-inflammatory and neuroprotective effects. We hypothesized that aerobic exercise could attenuates memory deficits by regulating inflammatory status. PURPOSE: To investigate whether regular aerobic exercise regulate inflammation and attenuate memory deficits induced by Aβ1-42 in rat. METHODS: Sprague-Dawley rats were divided into 3 groups: control group (C), Aβ1-42 infusion group (A), Aβ1-42 infusion with exercise group (E). Rats in group A and E were injected 10μg Aβ1-42 oligomer (1μg/μl saline) into their hippocampus, and rats from group C were injected with an same volume of saline. The rats in group E underwent aerobic exercise training on a leveled motorized treadmill at a moderate speed for consecutive 5 weeks (once a day, 6 days/week) starting at the 2nd day after Aβ1-42 injection. The memory ability was evaluated by Morris Water Maze (MWM) and the inflammatory status was analyzed by expressions levels of proinflammatory cytokines (TNF-α, IL-1β) and anti-inflammatory cytokine (TGF-β, IL-10) in hippocampus using Western Blot. RESULTS: MWM test showed that memory functions of rats were impaired by Aβ1-42 infusion, but this impairment was ameliorated by aerobic treadmill exercise. Compared with group C, both pro-inflammatory and anti-inflammatory cytokines in group A increased by different degrees (TNF-α: 306.9%, IL-1β: 255.6%, TGF-β: 78.3%, IL-10: 80.0%). Compared with group A, the expression of TNF-α and IL-1β in group AE decreased by 31.4% and 25.0%, whereas TGF-β and IL-10 increased by 68.5% and 39.0% respectively. CONCLUSIONS: The findings demonstrated that treadmill exercise could adjust inflammation status in hippocampus and attenuate the cognitive impairment of rats induced by Aβ1-42. Supported by the Fundamental Research Funds for the Central Universities,Southwest University for Nationalities (2018NQN19) and the Sichuan Science and Technology Project (18YYJC1355).
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