Scheuermann Britton, Nichol Kathryn, Levenson Cathy, Schulze Kiana, Vied Cynthia, Woodman Christopher, Prisby Rhonda, Reyes Rafael, Evanson Kirk, Kuo Lih, Ade Carl, Muller-Delp Judy
Department of Kinesiology, Kansas State University, Manhattan, KS, USA.
Institute for Brain Aging and Dementia, University of California at Irvine, Irvine, CA, USA.
J Physiol. 2025 Aug 6. doi: 10.1113/JP288866.
The ageing global population is experiencing an increased prevalence of cerebrovascular diseases, such as stroke and dementia. This highlights a need for understanding the pathophysiological mechanisms of age-related cerebrovascular alterations, alongside benefits of interventions such as physical activity. Therefore, our aims were to: (1) examine the impact of ageing and exercise training on cerebrovascular function and (2) to characterize age- and exercise training-related changes in the hippocampus transcriptome. Young and old male rats were randomized to a sedentary condition or exercise training for 10 weeks. In the first protocol, cerebral arteries were isolated to test vasomotor reactivity, quantify gene/protein expression and assess nitric oxide production. In the second protocol, anhedonia was assessed and hippocampal tissue collected for RNA-sequencing. Bioinformatic analyses (i.e. protein-protein interaction mapping) were performed. Ageing impaired endothelium-dependent vasoreactivity in the posterior communicating artery (PCoA), with a shift from endothelial nitric oxide synthase (NOS)- to neuronal NOS-mediated vasorelaxation, as well as alterations in oxidative stress production. In support, PCoA superoxide-mediated vasoreactivity and neuronal NOS-mediated production of NO decreased with age. Exercise enhanced vasodilatation in young rats, but the results suggested reduced cerebrovascular plasticity in older animals. In the second protocol, exercise training attenuated the age-related increase in anhedonia behaviour. Hippocampal RNA-sequencing revealed altered inflammatory and oxidative stress pathways with ageing that were mitigated by exercise training. Our findings underscore the complex interplay between vascular/neuronal factors in the ageing brain. Furthermore, these findings highlight the therapeutic potential of exercise in mitigating the adverse effects of ageing on cerebral health. KEY POINTS: Ageing is associated with increased risks of cerebrovascular disease and neurocognitive decline. Little is known about the underlying mechanisms involved in this process, limiting our ability to design appropriate interventions. Ageing is associated with alterations in cerebrovascular function, including possible changes in the mechanisms underlying vasomotor reactivity. Hippocampal RNA-seq revealed age-related alterations in neuronal, vascular, immune and oxidative-stress related signalling pathways. Exercise training may have mitigated many of these age-related changes, suggesting that enhancing physical activity may be a feasible means to preserve cerebral health in older individuals.
全球人口老龄化使得脑血管疾病(如中风和痴呆症)的患病率不断上升。这凸显了了解与年龄相关的脑血管改变的病理生理机制以及诸如体育活动等干预措施益处的必要性。因此,我们的目标是:(1)研究衰老和运动训练对脑血管功能的影响,以及(2)描述海马体转录组中与年龄和运动训练相关的变化。将年轻和年老的雄性大鼠随机分为久坐组或进行10周的运动训练组。在第一个方案中,分离脑动脉以测试血管运动反应性、量化基因/蛋白质表达并评估一氧化氮的产生。在第二个方案中,评估快感缺失情况并收集海马体组织用于RNA测序。进行了生物信息学分析(即蛋白质 - 蛋白质相互作用图谱分析)。衰老损害了后交通动脉(PCoA)的内皮依赖性血管反应性,导致从内皮型一氧化氮合酶(NOS)介导的血管舒张转变为神经元型NOS介导的血管舒张,同时氧化应激产生也发生改变。此外,PCoA中超氧化物介导的血管反应性和神经元型NOS介导的NO产生随年龄增长而降低。运动增强了年轻大鼠的血管舒张,但结果表明老年动物的脑血管可塑性降低。在第二个方案中,运动训练减轻了与年龄相关的快感缺失行为增加。海马体RNA测序显示,衰老会改变炎症和氧化应激途径,而运动训练可减轻这些改变。我们的研究结果强调了衰老大脑中血管/神经元因素之间复杂的相互作用。此外,这些发现突出了运动在减轻衰老对大脑健康不利影响方面的治疗潜力。要点:衰老与脑血管疾病风险增加和神经认知能力下降有关。对于这一过程中涉及的潜在机制知之甚少,这限制了我们设计适当干预措施的能力。衰老与脑血管功能改变有关,包括血管运动反应性潜在机制的可能变化。海马体RNA测序揭示了与年龄相关的神经元、血管、免疫和氧化应激相关信号通路的改变。运动训练可能减轻了许多与年龄相关的这些变化,这表明增加体育活动可能是维持老年人脑健康的一种可行方法。