从神经炎症到神经保护:关注认知障碍潜在的新治疗靶点

A. Cotroneo, P. Gareri, Valeria Graziella Laura Manfredi
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引用次数: 1

摘要

神经变性与神经炎症密切相关。它通常与氧化应激和细胞能量代谢的有意义的变化有关。神经炎症是由于非神经元细胞(小胶质细胞、星形胶质细胞、肥大细胞)的激活和增殖引起的。此外,它与促炎物质的释放有关,能够改变突触的可塑性。小胶质细胞和星形胶质细胞的激活导致毒物释放(活性氧、炎性细胞因子);然而,这一过程的最终目标是胆碱能神经元。许多物质可以促进神经保护;最近的科学证据集中在sirtuins的作用上。特别是,SIRT1被热量限制、NAD生物合成和不同的激活剂(称为STACs)激活。胞胆碱是最强大的stacs之一。它已被广泛证明具有神经保护作用,许多研究加强了它可能的作用。
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From Neuroinflammation to Neuroprotection: Focus on Potential New Therapeutic Targets in Cognitive Impairment
Neurodegeneration is closely linked to neuroinflammation. It is often associated with oxidative stress and meaningful changes in cell energy metabolism. Neuroinflammation is due to non-neuronal cell activation (microglia, astrocytes, mast cells) activation and proliferation. Also, it is associated with pro-inflammatory substances release, able to modify synaptic plasticity. Microglia and astrocytes activation lead to toxic agent’s release (reactive oxygen species, inflammatory cytokines); however, the final target of this process is the cholinergic neuron. A number of substances can promote neuroprotection; recent scientific evidence focuses on the role of sirtuins. In particular, SIRT1 is activated by caloric restriction, NAD biosynthesis and different activators, called STACs (Sirtuin Activating Compounds). Citicoline is one of the most powerful STACs. It has been widely shown to possess neuroprotective action, and lots of studies strengthened its possible role.
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