Methamphetamine- and trauma-induced brain injuries: comparative cellular and molecular neurobiological substrates.
Methamphetamine- and trauma-induced brain injuries: comparative cellular and molecular neurobiological substrates.
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DOI：
10.1016/j.biopsych.2009.02.021
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发表时间：
2009-07-15
影响因子：
10.6
通讯作者：
Cadet, Jean Lud
中科院分区：
文献类型：
--
作者：
Gold, Mark S.;Kobeissy, Firas H.;Wang, Kevin K. W.;Merlo, Lisa J.;Bruijnzeel, Adriaan W.;Krasnova, Irina N.;Cadet, Jean Lud
关键词：
甲基苯丙胺（冰毒）的使用是一个日益严重的公共卫生问题，因为它的滥用与对人类大脑的长期生化和结构影响有关。机械性损伤（如创伤性脑损伤，TBI）和缺血性损伤（中风）通常会导致人类神经退行性变。在这篇综述中，我们讨论了最近的研究结果，证明精神兴奋剂药物，甲基安非他明，可以导致几个大脑区域的神经元损伤。从我们的实验室和其他研究人员积累的证据表明，急性给药甲基安非他明导致钙蛋白酶和半胱天冬酶蛋白水解系统的激活。这些系统也参与造成继发于创伤性和缺血性脑损伤的神经元损伤。蛋白酶的激活伴随着内源性神经元结构蛋白（α ii -谱蛋白和MAP-tau蛋白）的蛋白水解，这些损伤后它们的分解产物的出现证明了这一点。综上所述，这些观察结果表明，冰毒暴露，就像TBI一样，可以通过在一生中使用大剂量毒品的冰毒成瘾者的大脑中引起细胞凋亡和坏死细胞死亡，对大脑造成实质性损害。最后，由于冰毒滥用与TBI患者相似，伴随着大脑功能和结构的变化，如果冰毒成瘾者的治疗更加强调康复，并结合使用潜在的神经保护药理学药物，如钙蛋白酶和半胱天酶抑制剂，与TBI患者类似，可能会获得更大的益处。
The use of methamphetamine (METH) is a growing public health problem because its abuse is associated with long-term biochemical and structural effects on the human brain. Neurodegeneration is often observed in humans as a result of mechanical injuries (e.g. traumatic brain injury, TBI) and ischemic damage (strokes). In this review, we discuss recent findings documenting the fact that the psychostimulant drug, METH, can cause neuronal damage in several brain regions. The accumulated evidence from our laboratories and those of other investigators indicates that acute administration of METH leads to activation of calpain and caspase proteolytic systems. These systems are also involved in causing neuronal damage secondary to traumatic and ischemic brain injuries. Protease activation is accompanied by proteolysis of endogenous neuronal structural proteins (αII-spectrin and MAP-tau protein) evidenced by the appearance of their breakdown products after these injuries. When taken together, these observations suggest that METH exposure, like TBI, can cause substantial damage to the brain by causing both apoptotic and necrotic cell death in the brains of METH addicts who use large doses of the drug during their lifetimes. Finally, because METH abuse is accompanied by functional and structural changes in the brain similar to those in TBI, METH addicts might experience greater benefit if their treatment involved greater emphasis on rehabilitation in conjunction with the use of potential neuroprotective pharmacological agents such as calpain and caspase inhibitors similar to those used in TBI.
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