Inorganic Mercury and Alzheimer's Disease-Results of a Review and a Molecular Mechanism

Mercury has been introduced into the human environment in large quantities through industrial and medical processes, starting in the early nineteenth century. It is one of the most toxic substances known. Circumstantial evidence suggests that the pathology of Alzheimer's disease (AD) might be in part caused or exacerbated by inorganic mercury (IM). We therefore present here the results of a systematic review, covering 106 studies, most of them case control and cohort studies. Thirty-two studies, out of 40 testing memory in individuals exposed to IM, 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 and animal models showed that IM reproduces all pathological changes seen in AD. Its high affinity for selenium and selenoproteins suggests that IM may promote neurodegenerative disorders via disruption of redox regulation. IM may therefore play a role as a co-factor in the multi-factorial development of AD. It may also increase the pathological influence of other metals already known to play a potential role in AD, such as aluminum, copper, or iron. The mechanistic model provided here explains the considerable delay until clinical symptoms can be seen. Mercury should be eliminated from biological cycles as quickly as possible.