"我们发现，慢性疼痛会改变DNA标记的方式，不仅涉及大脑，还涉及T细胞。T细胞是一种对免疫力至关重要的白细胞"麦吉尔大学医学院教授Moshe Szyf说，"我们的发现强调了慢性疼痛对身体其他重要部分比如免疫系统的毁灭性影响。"

        慢性疼痛--持续6个月或更长时间的疼痛--是全球范围内导致残障的最常见原因之一。尽管研究人员在寻找新疗法策略的工作中付出了巨大的努力，但是，慢性疼痛的有效疗法仍然难以捉摸。

        使用大鼠模型

        麦吉尔团队使用一种通过化学甲基(methyl group)标记绘制DNA的方法研究了来自大鼠大脑和白细胞的DNA。"甲基标记对调控这些基因如何工作是重要的"共同作者、牙科教授、Alan Edwards疼痛研究中心研究员Laura Stone解释道。这种化学标记是不断发展的表观遗传学领域的一部分，涉及"开启"或"关闭"基因的修饰，有效地重新编程它们的工作方式。

        "我们惊讶于被慢性疼痛标记的基因的数量--成百上千的不同基因被改变了"Szyf补充说，"现在我们可以考虑慢性疼痛对其他我们通常不会与疼痛相联系的身体系统的可能影响。"

        新型止痛药可能的靶点

        这些发现可能开辟人类慢性疼痛诊断和治疗的新路径，研究人员表示，随着对一些慢性疼痛标记的基因的发现，可能也代表着止痛药的新靶点。(生物谷Bioon.com)

        Overlapping signatures of chronic pain in the DNA methylation landscape of prefrontal cortex and peripheral T cells

        We tested the hypothesis that epigenetic mechanisms in the brain and the immune system are associated with chronic pain. Genome-wide DNA methylation assessed in 9 months post nerve-injury (SNI) and Sham rats， in the prefrontal cortex (PFC) as well as in T cells revealed a vast difference in the DNA methylation landscape in the brain between the groups and a remarkable overlap (72%) between differentially methylated probes in T cells and prefrontal cortex. DNA methylation states in the PFC showed robust correlation with pain score of animals in several genes involved in pain. Finally， only 11 differentially methylated probes in T cells were sufficient to distinguish SNI or Sham individual rats. This study supports the plausibility of DNA methylation involvement in chronic pain and demonstrates the potential feasibility of DNA methylation markers in T cells as noninvasive biomarkers of chronic pain susceptibility.