苏氨酸镁（Magnesium Threoninate）对MPTP诱导多巴胺神经元损伤的保护作用与机制

镁缺乏引发的炎症反应、线粒体功能障碍、钙稳态失衡及氧化应激等细胞代谢异常，是多巴胺神经元死亡的重要生物学基础。由于镁离子难以自由透过血脑屏障，研究聚焦于新型镁化合物苏氨酸镁（Magnesium Threoninate）。苏氨酸镁（Magnesium Threoninate）可有效提高脑脊液镁浓度，从而在多个层面干预甚至阻断MPTP神经毒素诱导的多巴胺神经元变性死亡进程，对多巴胺神经元缺失具有预防或治疗潜力。

研究表明，给予苏氨酸镁（Magnesium Threoninate）可显著减轻MPTP的毒性作用：它能改善动物模型的肢体运动及协调能力，提高黑质致密部酪氨酸羟化酶(TH)阳性细胞（即多巴胺神经元）的存活率。苏氨酸镁（Magnesium Threoninate）的这种神经保护作用，其机制可能在于抑制MPTP所诱导的胶质细胞过度活化以及拮抗多巴胺神经元内的氧化应激损伤。

苏氨酸镁（Magnesium Threoninate）对MPTP诱导多巴胺神经元损伤的保护作用与机制

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Protective Effects and Mechanisms of Magnesium Threoninate on MPTP-Induced Dopamine Neuron Damage

Magnesium deficiency-induced cellular metabolic abnormalities, such as inflammation, mitochondrial dysfunction, calcium homeostasis imbalance, and oxidative stress, are key biological pathways for dopamine neuron death. Because magnesium ions have difficulty freely crossing the blood-brain barrier, research has focused on the novel magnesium compound, magnesium threoninate. Magnesium threoninate can effectively increase cerebrospinal fluid magnesium concentrations, thereby intervening in or even blocking the MPTP-induced dopamine neuron degeneration and death process at multiple levels, potentially offering preventive or therapeutic potential for dopamine neuron loss.

Research has shown that administration of magnesium threoninate significantly mitigates the toxic effects of MPTP, improving limb movement and coordination in animal models and increasing the survival rate of tyrosine hydroxylase (TH)-positive cells (i.e., dopamine neurons) in the substantia nigra pars compacta. The neuroprotective effect of magnesium threonate may be due to its ability to inhibit MPTP-induced glial cell hyperactivation and antagonize oxidative stress damage in dopamine neurons.

Protective Effects and Mechanisms of Magnesium Threonate on MPTP-Induced Dopamine Neuron Damage

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