Microplastics and nanoplastics are accumulating worldwide. These particles, which largely come from single-use styrofoam, are now found in our environment, food, and water. Normal plastics break down naturally in the environment without the use of chemicals, and over time, they can degrade into microplastics and nanoplastics. Scientists are particularly concerned about the long-term health impacts of nanoplastics because they can enter the bloodstream, cross the blood-brain barrier, and accumulate in the brain. This buildup could cause health risks such as neurological damage.
Researchers have found that some nanoplastics prevent proteins from clumping together, while others cause them to form larger clusters that disrupt normal cell activity. Many of these scientists tested nanoplastics that were intentionally created for experimental purposes, known as modified nanoplastics. Modified nanoplastics have special surface coatings that help them bind proteins or enter cells, so they’re different from the particles humans are exposed to in the natural environment. Because these earlier researchers used artificial particles and simple cell systems, scientists remain uncertain whether natural nanoplastics could also affect brain health.
In particular, scientists have not yet examined whether specific nanoplastics that carry a negative electrical charge can enter brain cells. Due to their small size and charge, these particles travel through the body more easily and could even cross the blood–brain barrier, which normally protects the brain from harmful substances.
Researchers at Duke University recently tested whether negatively-charged nanoplastics derived from plastic foam, known as polystyrene, could affect proteins that cause Parkinson’s disease. They reasoned that the negative charge on these nanoplastics could allow them to strongly bind to a brain protein called Ɑ-synuclien, which is a molecular hallmark of Parkinson’s disease.
The researchers explained that Ɑ-synuclien becomes harmful when it clumps together, damaging dopamine-producing neurons and contributing to the movement problems seen in people with Parkinson’s. They hypothesized that once inside the brain, polystyrene nanoplastics could speed up the spread and aggregation of Ɑ-synuclein, potentially triggering early Parkinson’s symptoms, like tremors and slowed movement.
To test this, the team first mixed purified Ɑ-synuclein with polystyrene nanoplastics in a test tube and observed protein clumping over 24 days. Then they used a fluorescence microscope to monitor the uptake of negatively charged nanoplastics in lab-grown mouse neurons over 12 to 28 hours. Finally, they examined how the nanoplastics affected living mouse brains over 3 days to 2 months. The researchers used this step-by-step approach to study how the proteins and nanoparticles interacted, from molecular binding all the way to brain-level effects.
The researchers found that the negatively charged nanoplastics formed strong bonds with Ɑ-synuclein, causing it to clump much faster than normal. Inside the neurons, the nanoplastics interfered with the cells’ ability to break down waste, making it harder to clear out toxic protein buildup. Over time, this led to the formation of Ɑ-synuclein inclusions in the mouse brains, similar to protein deposits seen in Parkinson’s disease. These findings showed that environmental nanoplastics can worsen Ɑ-synuclein aggregation and produce early Parkinson’s-like changes in the brain.
The team concluded that nanoplastics are an emerging environmental risk factor for neurological diseases. Their discovery links a widespread pollutant to a major human health concern and shows how everyday plastic waste can influence the development of brain disorders. Scientists want to further understand this connection so they can evaluate the risk of nanoplastic exposure and develop better strategies to reduce it. They suggested that future researchers investigate whether similar brain effects occur in humans and how lowering plastic pollution might decrease these health risks.
