Imagine your brain as a city, with buildings representing cognitive function and bustling streets symbolizing synaptic plasticity. In Alzheimer’s disease (AD), this city loses its vitality as cognitive decline sets in. However, a systematic review and meta-analysis explored the effects of exercise on AD animal models, aiming to bring life back to the city. The studies found that exercise had a powerful impact, reducing escape latency and increasing platform crossover numbers and time in the target quadrant. Additionally, exercise increased the expression of PSD95, an important protein for synaptic function. Interestingly, starting exercise before the onset of AD seemed to have a greater effect compared to exercising after the disease had progressed. In fact, treadmill running proved to be a suitable exercise type for improving brain function. These findings imply that exercise holds great potential in improving cognitive function and preserving synaptic plasticity in AD. So grab your sneakers and start exercising! Want to dive deeper into this fascinating research? Check out the full article.

IntroductionCognitive decline is a central manifestation of Alzheimer’s disease (AD), and its process is inseparable from changes in synaptic plasticity. The aim of this review was to summarize and evaluate the effectiveness of exercise on cognitive function and synaptic plasticity in AD animal models.Materials and methodsEligible studies were searched from PubMed, MEDLINE, EMBASE, Web of Science, and Cochrane Library from April to May 2022. The risk of bias was evaluated by Systematic Review Centre for Laboratory Animal Experimentation (SYRCLE). The Morris water maze (MWM) test and synaptic plasticity were considered outcome measures. Data were analyzed using random-effects meta-analyses using the software Stata. Heterogeneity was examined by using I2 test. Sensitivity analysis and publication bias were also assessed.ResultsA total of 20 randomized controlled studies were eligible for study inclusion. Compared with controls, exercise decreased escape latency (SMD = −0.86, 95% CI: −1.21 to −0.50, P < 0.001), increased platform crossover numbers (SMD = 1.34, 95% CI: 0.57–2.11, P = 0.001) and time in the target quadrant (SMD = 1.65, 95% CI: 0.95–2.36, P < 0.001) and the expression of PSD95 (SMD = 0.73, 95% CI: 0.25–1.21, P = 0.003) in AD animals. The results of the subgroup analysis showed that exercise before AD had a greater effect on escape latency (SMD = −0.88, 95% CI: −1.25 to −0.52, P < 0.001), platform crossover numbers (SMD = 1.71, 95% CI: 1.23–2.18, P < 0.001), time in the target quadrant (SMD = 2.03, 95% CI: 1.19–2.87, P < 0.001) and the expression of PSD95 (SMD = 0.94, 95% CI: 0.19–1.69, P = 0.014) than exercise after AD. The results of the subgroup analysis also showed that treadmill running might be an appropriate exercise type.ConclusionOur findings suggested that exercise had a potential effect on improving cognitive function and synaptic plasticity. It can play a better neuroprotective role before AD.Systematic review registrationPROSPERO, identifier: CRD42022328438.

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