A Hypothesis and Evidence That Mercury May be an Etiological Factor in Alzheimer’s Disease
Robert Siblerud,
Joachim Mutter,
Elaine Moore,
Johannes Naumann and
Harald Walach
Additional contact information
Robert Siblerud: Rocky Mountain Research Institute, 9435 Olsen Court, Wellington, CO 80549, USA
Joachim Mutter: Environmental Medicine, 78467 Konstanze, Germany
Elaine Moore: Memorial Hospital, Colorado Springs, CO 80549 (Retired), USA
Johannes Naumann: European Institute for Physical Therapy and Balneology, Stadtsr 7, D-79104 Freiburg, Germany
Harald Walach: Department of Psychology, University Witten-Herdecke, 58455 Witten, Germany
IJERPH, 2019, vol. 16, issue 24, 1-15
Abstract:
Mercury is one of the most toxic elements and causes a multitude of health problems. It is ten times more toxic to neurons than lead. This study was created to determine if mercury could be causing Alzheimer’s disease (AD) by cross referencing the effects of mercury with 70 factors associated with AD. The results found that all these factors could be attributed to mercury. The hallmark changes in AD include plaques, beta amyloid protein, neurofibrillary tangles, phosphorylated tau protein, and memory loss—all changes that can be caused by mercury. Neurotransmitters such as acetylcholine, serotonin, dopamine, glutamate, and norepinephrine are inhibited in patients with Alzheimer’s disease, with the same inhibition occurring in mercury toxicity. Enzyme dysfunction in patients with Alzheimer’s disease include BACE 1, gamma secretase, cyclooxygenase-2, cytochrome-c-oxidase, protein kinases, monoamine oxidase, nitric oxide synthetase, acetyl choline transferase, and caspases, all which can be explained by mercury toxicity. Immune and inflammatory responses seen in patients with Alzheimer’s disease also occur when cells are exposed to mercury, including complement activation, cytokine expression, production of glial fibrillary acid protein antibodies and interleukin-1, transforming growth factor, beta 2 microglobulins, and phosphodiesterase 4 stimulation. Genetic factors in patients with Alzheimer’s disease are also associated with mercury. Apolipoprotein E 4 allele increases the toxicity of mercury. Mercury can inhibit DNA synthesis in the hippocampus, and has been associated with genetic mutations of presenilin 1 and 2, found in AD. The abnormalities of minerals and vitamins, specifically aluminum, calcium, copper, iron, magnesium, selenium, zinc, and vitamins B1, B12, E, and C, that occur in patients with Alzheimer’s disease, also occur in mercury toxicity. Aluminum has been found to increase mercury’s toxicity. Likewise, similar biochemical factors in AD are affected by mercury, including changes in blood levels of homocysteine, arachidonic acid, DHEA sulfate, glutathione, hydrogen peroxide, glycosamine glycans, acetyl-L carnitine, melatonin, and HDL. Other factors seen in Alzheimer’s disease, such as increased platelet activation, poor odor identification, hypertension, depression, increased incidences of herpes virus and chlamydia infections, also occur in mercury exposure. In addition, patients diagnosed with Alzheimer’s disease exhibit higher levels of brain mercury, blood mercury, and tissue mercury in some studies. The greatest exogenous sources of brain mercury come from dental amalgams. Conclusion: This review of the literature strongly suggests that mercury can be a cause of Alzheimer’s Disease.
Keywords: Alzheimer’s disease; mercury; etiology (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2019
References: View complete reference list from CitEc
Citations: View citations in EconPapers (4)
Downloads: (external link)
https://www.mdpi.com/1660-4601/16/24/5152/pdf (application/pdf)
https://www.mdpi.com/1660-4601/16/24/5152/ (text/html)
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:gam:jijerp:v:16:y:2019:i:24:p:5152-:d:298770
Access Statistics for this article
IJERPH is currently edited by Ms. Jenna Liu
More articles in IJERPH from MDPI
Bibliographic data for series maintained by MDPI Indexing Manager ().