A new study has raised alarms about the potential link between micro- and nanoplastics and the development of Alzheimer’s disease, suggesting that these ubiquitous environmental pollutants may contribute to cognitive decline. The findings come from researchers at the University of Rhode Island’s College of Pharmacy, who tested how plastic particles interact with the brain in mice.

Microplastics in everyday life

Micro- and nanoplastics, tiny fragments of plastic prevalent in the environment, regularly enter the human body. They are found in the water we drink, the food we eat, and even the air we breathe. While earlier research confirmed that microplastics can infiltrate all systems of the body—including the blood-brain barrier, a natural defense that protects the brain from harmful pathogens—this new study takes the concern further by directly connecting their presence to Alzheimer’s-like symptoms.

Focus on genetic risk

The study, published in Environmental Research Communications, examined mice genetically modified to carry the APOE4 gene, a well-known risk factor for Alzheimer’s disease. Individuals with this gene are 3.5 times more likely to develop the condition than those carrying the APOE3 variant.

“In these mice, like in people, it’s not a guarantee that you’re going to see any changes in cognition,” explained Jaime Ross, assistant professor of pharmacy at the University of Rhode Island. “You could have identical twins, both carrying APOE4, one totally cognitively healthy, and the other could develop Alzheimer’s disease. That tells us lifestyle and environmental factors play a role.”

Ross and her team specifically wanted to know: if someone carries the APOE4 gene and is also exposed to high levels of microplastics, could this combination accelerate Alzheimer’s onset?

Testing and results

To explore this, the researchers exposed the mice to micro- and nanoplastics and then observed their cognitive behaviors.

The findings revealed sex-dependent differences similar to those seen in human Alzheimer’s patients.

“In human patients, men often show more changes in apathy—they care less—while women experience greater memory loss. When we exposed these mice carrying the Alzheimer’s risk gene to plastics, we saw behavior changes that matched these sex-specific patterns,” Ross said.

The implication is that microplastics not only accumulate in the brain but may also trigger behavioral and cognitive effects resembling early Alzheimer’s.

A call for deeper research

The results, while preliminary, are significant enough to warrant further investigation. Alzheimer’s is a complex disease influenced by genetics, lifestyle, and environment, and the study underscores the possibility that microplastics could be a key environmental toxin influencing its development.

“There are modifiable factors related to Alzheimer’s—diet, exercise, vitamins, and now environmental toxins like microplastics,” Ross added. “If exposure to these plastics is confirmed as a contributing factor, reducing or eliminating them could become an important step in prevention.”

With microplastics already considered one of the most prominent pollutants in daily life, this study highlights an urgent need to examine their long-term effects on human health.

While more research is required to establish a definitive link, the early evidence paints a troubling picture of how pervasive plastic pollution may extend far beyond environmental damage—directly impacting human cognitive health.