Findings from a new animal study suggest that exposure to cadmium, a neurotoxin, leads to accelerated cognitive impairment. Males with a genetic risk factor for developing Alzheimer’s disease are particularly vulnerable.

A toxic heavy metal and a known carcinogen, cadmium is released into the environment both naturally and via human activity. It is particularly present in cigarette smoke as well as a byproduct of manufacturing and construction processes. Beyond there though, it is also amasses on leafy vegetables and rice, meaning that even non-smokers are at risk of exposure.

According to the author of the study, Zhengui Xia, “This heavy metal is bad for you...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.”





Although researchers have known that presence of the E4 allele of the apolipoprotein E (APOE) gene leads to an increased risk of developing Alzheimer’s, having this gene alone is not enough to develop the disease. Thus, researchers from the University of Washington conducted experiments on mice holding the gene to see how exposure to cadmium impacts their cognitive functioning. For around 3 months, they fed the mice low doses of the toxin in their drinking water, monitoring cadmium levels in their blood to ensure they were within the range of levels seen in the US general population.

At the end of the study, the researchers found that cadmium exposure impaired short-term spatial working memory, with these impairments being seen from as early as 3 weeks of exposure. Other cognitive impairments occurred too, including changes in behavior while navigating a T-maze, suggesting an interaction between the gene APOE E4 and cadmium to result in long-lasting changes in the brain.

On how this may happen, the researchers wrote, “It is possible that APOE E4 may cause leakage on the blood-brain barrier and lead to higher degree of cadmium accumulation in the APOE E4 brain.” The researchers also suggested that the interaction between the APOE E4 gene and cadmium may lead to reduced neurogenesis, or the production of new neurons, in the hippocampus, something vital for maintaining cognitive abilities later on in life.

Sources: University of Washington, Futurity and Oxford Academic