{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,29]],"date-time":"2026-08-29T02:27:31Z","timestamp":1787970451942,"version":"build-2784847793"},"reference-count":93,"publisher":"MDPI AG","issue":"24","license":[{"start":{"date-parts":[[2019,12,17]],"date-time":"2019-12-17T00:00:00Z","timestamp":1576540800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJERPH"],"abstract":"<jats:p>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\u2019s 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\u2014all changes that can be caused by mercury. Neurotransmitters such as acetylcholine, serotonin, dopamine, glutamate, and norepinephrine are inhibited in patients with Alzheimer\u2019s disease, with the same inhibition occurring in mercury toxicity. Enzyme dysfunction in patients with Alzheimer\u2019s 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\u2019s 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\u2019s 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\u2019s disease, also occur in mercury toxicity. Aluminum has been found to increase mercury\u2019s 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\u2019s 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\u2019s 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\u2019s Disease.<\/jats:p>","DOI":"10.3390\/ijerph16245152","type":"journal-article","created":{"date-parts":[[2019,12,20]],"date-time":"2019-12-20T03:19:36Z","timestamp":1576811976000},"page":"5152","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":75,"title":["A Hypothesis and Evidence That Mercury May be an Etiological Factor in Alzheimer\u2019s Disease"],"prefix":"10.3390","volume":"16","author":[{"given":"Robert","family":"Siblerud","sequence":"first","affiliation":[{"name":"Rocky Mountain Research Institute, 9435 Olsen Court, Wellington, CO 80549, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joachim","family":"Mutter","sequence":"additional","affiliation":[{"name":"Environmental Medicine, 78467 Konstanze, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elaine","family":"Moore","sequence":"additional","affiliation":[{"name":"Memorial Hospital, Colorado Springs, CO 80549 (Retired), USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes","family":"Naumann","sequence":"additional","affiliation":[{"name":"European Institute for Physical Therapy and Balneology, Stadtsr 7, D-79104 Freiburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harald","family":"Walach","sequence":"additional","affiliation":[{"name":"Department of Psychology, University Witten-Herdecke, 58455 Witten, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2019,12,17]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"34","DOI":"10.1186\/s13195-015-0118-1","article-title":"Is the risk of Alzheimer\u2019s disease and dementia declining?","volume":"7","author":"Langa","year":"2015","journal-title":"Alzheimer Res. 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