By: David A Fein, MD
Medical Director
Princeton Longevity Center
Microplastics and nanoplastics (MNPs) are tiny particles of plastic, less than 5 mm long but often too small to even be visible, that are either intentionally added to consumer goods or result from the breakdown of larger plastics. Today, these particles are everywhere in our environment. They easily pass through water filtration systems and accumulate in lakes and oceans, and are also found in the particulate air pollution. Multiple studies have shown that these particles enter the human body through ingestion, inhalation, and skin exposure and accumulate in and interact with tissues and organs like the placenta, lungs, liver, and blood. Now, a growing body of research suggesting possible links between microplastics (and especially nanoplastics) and effects on the brain, including neurodegenerative disorders.
Alarmingly high levels of microplastics accumulate in the human brain, at concentrations significantly higher than in other organs, and these levels have been increasing over time. Recent studies report brain microplastic/nanoplastic levels in non-dementia samples of about 3,000-5,000 µg per gram of frontal cortex tissue. That corresponds to several grams of plastic particles potentially in a human brain. So when media talk about “a spoon’s worth” (a few grams) of plastic particles already in your brain, that is in the ballpark of these rough extrapolations
A study from the University of New Mexico compared brain tissue samples from people who died in 2016 vs 2024, some of whom had dementia. They found microplastic (and nanoplastic) levels in the brain that were higher than in liver or kidney, and significantly higher in brains from dementia cases than those without dementia. Tissue samples from people with dementia had up to 10 times the accumulation of microplastics in their brains as those with no dementia diagnosis, The authors cautioned strongly that this is association, not proof of causation. For example, dementia could itself lead to changes (e.g. in blood-brain barrier integrity, or in brain clearance mechanisms) that increase accumulation.
Animal and cell-studies also point toward mechanisms consistent with worsening Alzheimer’s-like pathology after plastic or nanoparticle exposure. There are specific mouse strains that are used as research models for Alzheimer’s disease. In an experiment that exposed those mice to nanoplastics, the exposure increased amyloid-beta plaque deposition in their brains which may be an indication of increasing progression of Alzheimer’s disease.
Another study looked at a specific type of microplastic, polystyrene, and found that polystyrene microparticle promoted worsening cognitive impairment in mice with Alzheimer’s and also increased markers of inflammation in the brain.
Microplastics may also interact with other genetic risk factors for neurologic disease. A recent study explored how plastic exposure interacts with known Alzheimer’s risk genes, particularly APOE4 (which in humans is associated with higher Alzheimer’s risk). In mice carrying APOE4, microplastic exposure led to more rapid and increased cognitive declines, and changes in markers of brain inflammation.
On-going research has suggested several possible pathways that microplastics may damage brain and other tissues. Microplastics may increase production of reactive oxygen species leading to increased oxidative stress in neural tissue. The Increased evidence of inflammation in the nervous system that has been seen in many models may possibly be a result of the oxidative stress. There is also evidence that nanoparticles disrupt mitochondrial activity in neurons. Impaired mitochondrial function has been proposed as one of the underlying pathologies in Alzheimer’s, Parkinsons and other neurodegenerative diseases. And in some animal models microplastics lead to changes in levels or function of neurotransmitters.
All of this is concerning about the possible dangers of plastics accumulating in our brains. But there are some caveats. Most of the work has been done in animal models or cell cultures. Translating that to human disease is tricky. Additionally, the doses of particles used in some of the experimental models may not correspond to what humans are typically exposed to. And most important of all, correlation does not equal causation. We are not yet certain that the increased presence of plastics in the brain of people with neurodegenerative disease is the cause of the disease versus the higher levels being the result of pre-existing disease that simply makes it easier for the particles to enter the brain.
So, we are not yet at the point of being able to say there is proof that microplastics in the brain lead to neurodegenerative disease in humans. But there is reason for concern. Microplastics do get into the brain and may worsen the processes known to be involved in degenerative disease. It may take decades for more research to definitively prove the link between exposure and disease. But by then, it is likely you will have already accumulated a high burden of microplastics in your body and once they are in the brain, getting them out may be difficult. Taking steps now to limit your exposure to microplastics would appear to be a prudent investment in your future health.