Investigation on synucleinopathy and epigenetic mechanisms in the brains of methamphetamine abusers

这项研究表明，除了多巴胺能神经末梢标记缺陷和神经胶质反应，突触核蛋白病是由甲基苯丙胺神经毒性，包括氧化应激在甲基苯丙胺滥用者的大脑中诱导的。此外，我们已经证明，脑源性神经营养因子（BDNF）和甲基CpG结合蛋白2（MeCP 2），BDNF的转录因子，这是参与表观遗传学，发现在甲基苯丙胺滥用者。从法医病理学的角度来看，检测突触核蛋白病和表观遗传机制，涉及MeCP2和BDNF的表达可能是有用的，以调查涉及的机制，在人类甲基苯丙胺滥用者的神经毒性和药物依赖。

This study suggests that, in addition to dopaminergic terminal marker deficits and glial reactions, synucleinopathy is induced by methamphetamine neurotoxicity including oxidative stress in the brains of methamphetamine abusers. Furthermore, we have demonstrated that brain-derived neurotorophic factor (BDNF) and methyl CpG binding protein 2 (MeCP2), a transcription factor of BDNF, that is involved in epigenetics, are found in methamphetamine abusers. In the point of view of forensic pathology, detection of synucleinopathy and epigenetic mechanisms involving MeCP2 and BDNF expression could be useful to investigate the mechanisms involved in neurotoxicity and drug dependence of human methamphetamine abusers.