Department of Environmental and Integrative Medicine, Constance, Germany.
J Alzheimers Dis. 2010;22(2):357-74. doi: 10.3233/JAD-2010-100705.
Mercury is one of the most toxic substances known to humans. It has been introduced into the human environment and has also been widely used in medicine. Since circumstantial evidence exists that the pathology of Alzheimer's disease (AD) might be in part caused or exacerbated by inorganic mercury, we conducted a systematic review using a comprehensive search strategy. Studies were screened according to a pre-defined protocol. Two reviewers extracted relevant data independent of each other. One thousand and forty one references were scrutinized, and 106 studies fulfilled the inclusion criteria. Most studies were case control or comparative cohort studies. Thirty-two studies, out of 40 testing memory in individuals exposed to inorganic mercury, found significant memory deficits. Some autopsy studies found increased mercury levels in brain tissues of AD patients. Measurements of mercury levels in blood, urine, hair, nails, and cerebrospinal fluid were inconsistent. In vitro models showed that inorganic mercury reproduces all pathological changes seen in AD, and in animal models inorganic mercury produced changes that are similar to those seen in AD. Its high affinity for selenium and selenoproteins suggests that inorganic mercury may promote neurodegenerative disorders via disruption of redox regulation. Inorganic mercury may play a role as a co-factor in the development of AD. It may also increase the pathological influence of other metals. Our mechanistic model describes potential causal pathways. As the single most effective public health primary preventive measure, industrial, and medical usage of mercury should be eliminated as soon as possible.
汞是已知对人类最具毒性的物质之一。它已被引入人类环境，并且在医学中也得到了广泛应用。由于有间接证据表明阿尔茨海默病（AD）的病理学部分可能是由无机汞引起或加剧的，因此我们采用全面的搜索策略进行了系统评价。研究根据预先确定的方案进行筛选。两位评审员独立提取相关数据。对 1041 篇参考文献进行了详细审查，其中 106 项研究符合纳入标准。大多数研究是病例对照或比较队列研究。在 40 项测试接触无机汞个体记忆的研究中，有 32 项发现存在明显的记忆缺陷。一些尸检研究发现 AD 患者脑组织中的汞含量增加。血液、尿液、头发、指甲和脑脊液中汞水平的测量结果不一致。体外模型表明，无机汞可复制 AD 所见的所有病理变化，动物模型中无机汞产生的变化与 AD 相似。其与硒和硒蛋白的高亲和力表明，无机汞可能通过破坏氧化还原调节来促进神经退行性疾病。无机汞可能在 AD 的发展中起辅助因子的作用。它还可能增加其他金属的病理影响。我们的机制模型描述了潜在的因果途径。作为唯一最有效的公共卫生一级预防措施，应尽快消除汞在工业和医疗中的使用。
