Scientists Connect Alzheimer’s Disease To Mercury
International Academy of Oral Medicine and Toxicology
An Organization Dedicated to Evidence Based Health Care
P.O. Box 608531, Orlando, FL 32860-8531
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NEW RESEARCH CONNECTS MERCURY TO ALZHEIMER’S DISEASE!
Research conducted at the University of Calgary Faculty of Medicine has demonstrated that trace amounts of mercury can cause the type of damage to nerves that is characteristic of the damage found in Alzheimer’s Disease. The level of mercury exposure is consistent with those levels found in humans with mercury/silver amalgam dental fillings. The exposure to mercury caused the formation of “neurofibrillar tangles,” which are one of the two diagnostic markers for Alzheimer’s Disease. The scientists found that other metals, including aluminum, did not cause the damage. Previous research has shown that mercury can cause the formation of the other Alzheimer’s Disease diagnostic marker, “amyloid plaques.”
The research, published in a peer-reviewed medical journal, is accompanied by a video visual presentation of the effect. Utilizing digital time-lapse photography, this video shows rapid damage to the nerve cells after introduction of minute amounts of mercury. Funding for this video was provided by the International Academy of Oral Medicine and Toxicology (IAOMT).
SPECIAL NOTE: The University of Calgary has placed a copy of the video on their site at:
To view the video you will need “Quick Time” Player which can be dowloaded from the site if you do not have it.
This video will be available to media contacts (only) through:
Miss Karen Thomas
University of Calgary, Faculty of Medicine
T: 403-220-2945 F: 403-210-8141 Email: firstname.lastname@example.org
Media Embargo Date: 26 March 2001
Title: “Retrograde Degeneration of Neurite Membrane Structural Integrity of Nerve Growth Cones Following In Vitro Exposure To mercury.”
Authors: Leong, CW; Syed, NI; Lorscheider, FL.
Journal: NeuroReport, 12(4):733-737, 2001.
BIOPROBE COMMENT: This study should remove all doubt regarding the role that dental mercury from amalgam fillings plays in the development of Alzheimer’s Disease (AD). Although the American Dental Association would like to have you believe otherwise, science has clearly demonstrated that there is a positive correlation between brain mercury levels and the number and surfaces of “mercury/silver” amalgam dental fillings. The mercury levels that caused the devastating damage to nerve cells in the above referenced study were 100 to 1000 times below those found in the brains of people with “mercury/silver” amalgam dental fillings.
In 1997, researchers at the University of Calgary Medical School and the College of Pharmacy at the University of Kentucky clearly demonstrated that exposing rats to the same levels of mercury vapor that can be released from “mercury/silver” amalgam dental fillings caused the mercury to interact with brain tubulin and disassemble microtubles that maintain neurite structure. The identical neurochemical lesion of similar or greater magnitude is evident in Alzheimer brain homogenates from approximately 80% of patients, when compared to human age-matched neurological controls. (Neurotoxicology 1997;18(2):315-324)
In 2000, researchers at the Neurobiology Laboratory, Psychiatric University Hospital in Basel, Switzerland using neuroblastoma cells exposed to mercury demonstrated an increase in production of amyloid protein that makes up the amyloid plaques as well as significantly increasing the phophorylation of Tau protein. (J Neurochem 2000 Jan;74(1):231- 236)
Studies demonstrating a correlation between amalgam dental fillings and brain mercury levels:
Lakartidningen 1986 Feb 12;83(7):519-522
Swedish Dental Journal 1987;11(5):179-187
Sci Total Environ 1987 Oct;66:263-268
J Prosthet Dent 1987 Dec:58(6):704-707
FASEB J 1989 Dec;3(14):2651-2646
Sci Total Environ 1990 Dec 1;99(1-2):1-22
Sci Total Environ 1993 Sep 30;138(1-3):101-115
J Trace Elem Med Biol 1995 Jul;9(2):82-87
Zentralbl Hyg U:mweltmed 1996 Feb;198(3):275-291
FASEB J 1998 Aug;12(11):971-980
Biometals 1999 Sep;12(3):227-231