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Member Research & Reports

Member Research & Reports

Washington: New Evidence Links Cadmium Exposure to Key Alzheimer’s Gene, Accelerated Cognitive Decline

Exposure to the toxin cadmium, a known human carcinogen, even at levels found in people who do not smoke cigarettes, leads to accelerated cognitive impairment, according to a new animal study from the University of Washington School of Public Health. Those with genetic risk of developing Alzheimer’s disease, particularly males, are most vulnerable to the adverse health effects, the study suggests.

“This heavy metal is bad for you,” said corresponding author Dr. Zhengui Xia, professor in the Department of Environmental & Occupational Health Sciences at the University of Washington School of Public Health. “Exposure to cadmium through our daily lives could have a detrimental effect on our cognition. If you have the APOE E4 gene, the risk is significantly higher. Our study provides direct evidence for an interaction between this Alzheimer’s genetic risk gene and environmental exposures on accelerated cognitive impairment.”

Researchers used mouse models of Alzheimer’s disease that expressed either the E4 or E3 alleles of the human apolipoprotein E (APOE) gene, the well-known Alzheimer’s disease risk gene. To better understand the interaction between APOE E4 and cadmium exposure and the impact on cognition, mice were exposed to low-doses of cadmium through drinking water for about three months. The peak blood cadmium level seen in mice was within the range of levels found in the general population of the United States, including people who do not smoke. Novel object location tests were performed before, during and after cadmium exposure to probe the onset and persistence of memory impairment. T-maze tests were also conducted.

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