Mercury and Alzheimers---Food for thought Two articles in Pubmed:
Mercury induced the Accumulation of Amyloid Beta (Aß) in PC12 Cells: The Role of Production and Degradation of Aß., Song JW, Choi BS., Dec 2013, Department of Preventive Medicine, College of Medicine, Chung-Ang University, Seoul, Korea.
Abstract Extracellular accumulation of amyloid beta protein (Aß) plays a central role in Alzheimer's disease (AD). Some metals, such as copper, lead, and aluminum can affect the Aß accumulation in the brain. However, the effect of mercury on Aß accumulation in the brain is not clear. Thus, this study was proposed to estimate whether mercury concentration affects Aß accumulation in PC12 cells. We treated 10, 100, and 1000 nM HgCl2 (Hg) or CH3HgCl2 (MeHg) for 48 hr in PC12 cells. After treatment, Aß40 in culture medium increased in a dose- and time-dependent manner. Hg and MeHg increased amyloid precursor protein (APP), which is related to Aß production. Neprilysin (NEP) levels in PC12 cells were decreased by Hg and MeHg treatment. These results suggested that Hg induced Aß accumulation through APP overproduction and reduction of NEP.
Does inorganic mercury play a role in Alzheimer's disease? A systematic review and an integrated molecular mechanism., 2010 Mutter J1, Curth A, Naumann J, Deth R, Walach H.,Department of Environmental and Integrative Medicine, Constance, Germany.
Abstract "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."
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