Rajavand Hosniyeh, Zalouli Vahideh, Nematollahi Zeinab, Fathy-Karkaragh Farshid, Karimigharighi Elham, Jafarizadeh Farzad, Rabiei Rad Amirhossein
Regenerative Medicine Group (REMED), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
4UCL Department of Nanotechnology, Division of Surgery and Interventional Science, University College London, London, UK.
Mol Neurobiol. 2025 Apr 26. doi: 10.1007/s12035-025-04959-6.
Research has demonstrated that engaging in regular exercise has the potential to enhance cognitive function, promote neuroplasticity, and mitigate the likelihood of experiencing cognitive decline. The underlying mechanisms responsible for these effects are intricate and encompass various pathways, including the interaction between neurogranin and calmodulin. The activation of calcium signaling pathways is a significant mechanism through which regular exercise facilitates the treatment of age-related diseases. The activation of neurogranin and calmodulin induced by exercise can provide protection against neurodegeneration by promoting neuronal survival, mitigating oxidative stress, and improving mitochondrial function through the regulation of calcium homeostasis and energy metabolism. In addition, there is evidence suggesting that engaging in regular exercise can lead to an upregulation of neurotrophic factors, specifically brain-derived neurotrophic factor (BDNF). These factors are crucial for the survival of neurons, the plasticity of synapses, and overall cognitive function. Researchers have discovered the involvement of neurogranin in the regulation of BDNF signaling, underscoring its significance in exercise-induced neuroprotection and cognitive enhancement. The current work offers valuable insights into how neurogranin/calmodulin cooperation, facilitated by regular exercise, promotes the treatment of aging-related diseases. The results suggest that regular exercise could enhance memory, learning, synaptic plasticity, and resilience to neurological damage; promote recovery after brain injury; and treat aging-related disorders such as Alzheimer's disease.
研究表明，定期进行锻炼有可能增强认知功能、促进神经可塑性，并降低认知能力下降的可能性。造成这些影响的潜在机制错综复杂，涉及多种途径，包括神经颗粒素与钙调蛋白之间的相互作用。钙信号通路的激活是定期锻炼促进与年龄相关疾病治疗的一个重要机制。运动诱导的神经颗粒素和钙调蛋白的激活可以通过促进神经元存活、减轻氧化应激以及通过调节钙稳态和能量代谢来改善线粒体功能，从而为神经退行性变提供保护。此外，有证据表明，定期锻炼可导致神经营养因子上调，特别是脑源性神经营养因子（BDNF）。这些因子对神经元的存活、突触可塑性和整体认知功能至关重要。研究人员发现神经颗粒素参与了BDNF信号的调节，强调了其在运动诱导的神经保护和认知增强中的重要性。目前的研究工作为定期锻炼促进的神经颗粒素/钙调蛋白协同作用如何促进与衰老相关疾病的治疗提供了有价值的见解。结果表明，定期锻炼可以增强记忆、学习、突触可塑性以及对神经损伤的恢复能力；促进脑损伤后的恢复；并治疗与衰老相关的疾病，如阿尔茨海默病。
