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砷暴露是世界范围内的重要公共卫生问题。许多国家都一直受到砷中毒的威胁，地方性砷中毒病区的居民更是承受着疾病的痛苦。更值得注意的是，神经系统是砷中毒的靶器官。尽管已经存在一些关于砷神经毒性的可能理论，但确切的分子机制仍不明确。因此，明确发病机制，有效拮抗砷的神经毒性十分重要。有研究表明，砷可以影响许多组织及器官中的第10号染色体同源丢失性磷酸酶-张力蛋白(PTEN）、蛋白激酶B (Akt）和cAMP反应元件结合蛋白(CREB）的表达，并且PTEN/Akt/CREB信号通路在神经系统中发挥重要作用。因此，砷暴露引起的PTEN/Akt/CREB信号通路的变化对于研究砷神经毒性机制十分重要。“,”Arsenic pollution is a major public health problem worldwide. Many countries are threatened by arsenic poisoning for years and residents in endemic arseniasis areas suffer from the arsenic poisoning. More remarkable, researchers have pointed out that nervous system is the major target of arsenic. Though some possible theories of arsenic neurotoxicity have been proposed but the exact molecular mechanism is not clear yet. Exploring the exact mechanism is important, as we can antagonize arsenic neurotoxicity effectively. Previous evidences have shown that arsenic can influence the expressions of phosphatase and tensin homologue deleted on chromosome 10 (PTEN), protein kinase B (Akt) and cAMP-response element binding protein (CREB) in many tissues and organs, moreover, PTEN/Akt/CREB signaling pathway plays an important role in nervous system. Therefore, the dysfunction of PTEN/Akt/CREB signaling pathway induced by arsenic exposure is important to the research of the mechanism of arsenic neurotoxicity.