New evidence links cadmium exposure to Alzheimer's risk and accelerated cognitive decline.
While the toxin cadmium is well-known to play a role in kidney, bone and lung disease and to cause cancer in humans, new evidence from the lab of Zhengui Xia, PI on UW SRP Project 2, suggests that exposure to cadmium at relatively low levels also leads to accelerated cognitive impairment, particularly in those who are genetically predisposed to Alzheimer's disease.
The human apolipoprotein E (APOE) gene is well known among Alzheimer's researchers. When a person carries an E4 allele rather than the more common E3 allele, they show an increased risk for developing Alzheimer’s. However, simply having an E4 allele does not dictate that a person will develop the disease. Other, more poorly-understood risk factors, including environmental exposures, must interact with APOE E4 to increase Alzheimer’s risk.
The Xia lab conducted their study by exposing young mice to low levels of cadmium in their drinking water and then subjecting them to simple memory tests like novel object location tests and T-maze tests. They found that cadmium exposure impaired memory formation in all treated mice but that mice with the E4 gene were impacted most strongly, particularly male mice. Some of these effects did not show up until long after treatment had ceased.
This result supports a growing body of evidence that even relatively low levels of cadmium exposure can cause long-lasting impairment of cognitive function. The levels of cadmium that the mice were exposed to in this study created peak blood levels that are within the range of those seen in the blood of average, non-smoking Americans.