As you scroll through social media, bombarded by alarming posts about the dangers of plastic pollution on human health, you may find yourself grappling with feelings of helplessness and fear. In a world increasingly dominated by plastic consumption and production, the implications of our synthetic choices extend far beyond environmental degradation and wildlife harm. A recent study conducted in May 2024, still pending peer review, has sparked the science community with its troubling claim: micro- and nanoplastics (MNPs) have been detected in human brain tissue samples [1]. These minute fragments, measuring 500 micrometers down to 1 nanometer in diameter, arise from the breakdown of larger plastic items, infiltrating ecosystems and, alarmingly, our own bodies. As public concern over plastic pollution surges, amplified by mainstream news outlets and social media trends advocating extreme health-conscious behaviors, it becomes more evident that simply avoiding microplastics through dietary choices is nearly impossible. These particles can enter the human system via various pathways—ingestion, inhalation, and even dermal absorption—eventually accumulating in vital organs, including the brain [2].
Given this context, it is crucial for the scientific community to investigate the effects of MNPs on neurological health. Unlike other vital organs, the brain is central to cognition, emotion, and personality—integrating sensory information and experiences that shape our unique perspectives and identities. This makes it essential to investigate how microplastics affect the brain. The recent detection of these plastic particles in brain tissue samples underscores the urgent need for further research into their neurotoxic effects, potential links to neurodegenerative diseases, and broader implications for global health trends.
Detection of Plastics in Brain Tissue Samples
Matthew Campen, Regents’ Professor in the UNM Department of Pharmaceutical Sciences and researchers at the University of New Mexico established the first MNP in brain tissue study [1]. With approval from the University of New Mexico Office of the Medical Investigator, analysis was conducted on post-mortem samples of the human brain, liver, and kidney. Tissue samples were collected in 2016 and 2024, ensuring consistent methodology across both time points. First, the samples were preserved in formalin and treated with potassium hydroxide to break down their organic materials. Then, the remaining solid materials, mainly made of polymers, were separated using a high-speed centrifuge and analyzed to identify the specific types of polymers present. These advanced imaging techniques revealed accumulations of shard-like plastic particles less than 200 nm in length within the brain. Notably, the analysis revealed that MNPs were 7 to 30 times more concentrated in brain samples compared to liver and kidney tissues [1].

According to the study, researchers initially assumed that frontline organs like the kidney and liver would show higher concentrations of MNPs due to their role in responding to environmental toxins [1]. However, their findings challenged this assumption. Polyethylene is a synthetic material commonly used in everyday packaging such as plastic wraps, containers, bottles, and even household appliances and furniture. The spectrometry results revealed that 74% of all polymers found in the brain were polyethylene, which was greater than the polyethylene proportion of 44-57% in other organs like the liver and kidney [1]. This discrepancy may be attributed to the high speed at which these frontline organs metabolize foreign substances, effectively protecting the body. In contrast, the brain’s inability to detoxify and metabolize MNPs efficiently raises concerns, suggesting that exposure to MNPs may lead to more severe symptoms in the brain compared to the liver and kidney.
On a more microscopic level, as noted by Campen and researchers, polyethylene was the predominant polymer found in all sampled tissues and displayed similarly increasing trends from 2016 to 2024 in the liver and brain [1]. This indicates that the amount of polyethylene in these tissues has consistently increased over time alongside its commercial production increase (i.e. surges in plastic bottle production). The trends further support the relationship between exposure to polyethylene and its consequent increased accumulation in the body. However, the long-term clearance of these particles from the brain is still unclear [1].
Another potential mechanism for the infiltration of microplastics (MPs) into the brain is via the olfactory pathway. MPs can reach the olfactory bulb through multiple routes, with inhalation being a significant pathway. Tiny plastic particles present in the air can be inhaled into the nasal cavity, where they may penetrate the olfactory epithelium that is home to olfactory sensory neurons. From there, the neurons transmit signals to the olfactory bulbs above each nasal cavity, allowing MPs to enter the brain's neural pathways. A study led by Amato-Lourenço investigated the olfactory bulbs of 15 deceased individuals, obtained through routine coroner autopsies at the São Paulo City Death Verification Service, using spectroscopy to detect MPs [3]. The demographic characteristics of the study cohort included individuals with a median age of 69.5 years, ranging from 33 to 100 years, with 12 males and 3 females. Among the 15 individuals examined, eight showed evidence of MP presence in their olfactory bulbs. A total of 16 synthetic polymer particles and fibers were identified, primarily composed of polypropylene, a polymer distinct from polyethylene but commonly used alongside it in plastic packaging materials. Particle sizes ranging from 5.5 to 26.4 micrometers and an average fiber length of 21.4 micrometers were measured [3]. These findings suggest that the olfactory pathway may serve as a route for MPs to enter and build up in the brain, raising concerns about their potential neurological effects. The study underscores the urgent need for further research to investigate the health implications of MPs and their potential link to neurodegenerative diseases.
Mechanisms of Neurotoxicity
The neurotoxic effects of MNPs are a growing concern, particularly regarding their mechanisms in the brain. MNPs can cross the semipermeable membrane of the brain that separates circulating blood from the central nervous system, known as the blood-brain barrier, potentially exposing neurons to harm [4]. The selective permeability of the blood-brain barrier can allow lipophilic substances, including certain MNPs, to enter more easily and result in greater retention in the brain compared to other organs [5]. Unlike other organs that might have more robust detoxification and excretion pathways, the brain's blood-brain barrier structure can trap these particles, leading to long-term accumulation and potential chronic neurotoxic effects. The brain's high lipid (fats) content further contributes to the accumulation of MNPs, as lipids are hydrophobic and interact readily with the hydrophobic surfaces of MNPs. Overall, this combination of factors can contribute to MNP accumulation in brain tissue, heightening the risk of neurotoxicity and associated disorders.
A key mechanism of neurotoxicity that can be triggered by MNP exposure is oxidative stress, which occurs when the production of reactive oxygen molecular species exceeds the body's ability to neutralize them. The imbalance of oxygen species can lead to significant cellular damage and increased vulnerability to neuronal disorders. The neurotoxic effects of MNPs, particularly through oxidative stress and behavioral disruptions, present a significant risk to brain function and long-term neurological health. Recent research on polystyrene nanoplastics (PS-NPs) has shown that exposure to these small particles induces significant biochemical and behavioral changes in aquatic organisms, such as zebrafish [6]. PS-NPs were observed to accumulate in critical tissues, including the brain, liver, gonads, and intestines; PS-NPs showed a marked preference for brain tissue due to the particles' ability to cross biological membranes and persist in lipid-rich environments. Biochemical analysis revealed that PS-NPs exposure triggered oxidative stress, as evidenced by elevated levels of reactive oxygen species, and dysregulated neurotransmitter levels, including dopamine and serotonin. These changes point to potential neurotoxic effects, disrupting key neurochemical pathways and highlighting the risk to cognitive function and behaviors. In the zebrafish, exposure to PS-NPs resulted in behavioral disruptions, such as altered locomotion, aggression, and social behavior, as well as impairments in predator avoidance [6].
Additionally, MPs can inhibit acetylcholinesterase (AChE), the enzyme responsible for breaking down acetylcholine (ACh). ACh is a key neurotransmitter that helps transmit signals between neurons, but in excess can cause the overstimulation of receptors. Thus, AChE’s regulation of ACh is crucial as it allows neurons to reset and function properly, facilitating processes like memory, learning, and overall neural balance, maintaining healthy brain activity [7]. In a pilot study led by Luis Barboza, a team at the University of Porto investigated the potential presence of plastics in the brain of wild fish in relation to brain AChE activity. The study sought to explore the long-term exposure to pollution caused by a diversity of chemicals. Among the 60 European seabass specifically analyzed, 15% had MPs, with an average of 0.3 MPs per fish. The study also measured acetylcholinesterase activity, finding that fish with MPs showed lower AChE activity (80 nmol/nmol/min/mg protein) compared to those without MPs (117 nmol/nmol/min/mg protein). This significant difference suggests that MPs may negatively impact brain function by reducing AChE activity and disrupting normal neurotransmitter levels, potentially leading to increased cognitive dysfunction [7]. Behavioral and physiological consequences documented in fish exposed to MPs include a decrease in swimming performance, reduction of feeding activity, and neurite outgrowth from the cell body of neurons. This finding underscores the potential neurotoxic effects of microplastics, highlighting the need for further research to understand their impact on neural function and behavior across different species.
Alzheimer’s, Parkinson’s, and Related Dementia
Alzheimer’s Disease
MNPs are increasingly being studied for their potential effects on the nervous system, with research expanding into their role in a range of neurological diseases. Recent research has begun to explore the concerning link between MNPs and the progression of Alzheimer’s disease and related dementias. A study led by Wang highlights how exposure to the synthetic polymer polystyrene (PS) microplastics through inhalation, direct contact, or ingestion can exacerbate cognitive impairment in Alzheimer’s patients [8]. In the study, a total of 40 mice were divided into various groups: control, Alzheimer’s disease (AD) where the mice with mutations associated with early-onset Alzheimer's disease, and three PS treatment groups of increasing exposure concentrations. Each group consisted of 10 mice for behavioral tests, including the maze experiments that evaluated spatial learning and memory exploration abilities. The findings of the study revealed that exposure to PS significantly worsened cognitive abilities, which made it harder for the mice to find their way in tests designed to assess memory. The presence of PS also triggered harmful changes in microglia immune cells, leading to increased inflammation in the brain. This inflammation was indicated by higher levels of proteins that signal cell damage and stress. These effects were stronger with higher doses of PS, suggesting a direct link between the amount of microplastics and cognitive decline. Overall, the findings indicate that PS microplastics could play a role in worsening Alzheimer’s symptoms [8].
Jaime M. Ross, a neuroinflammation neuroscientist from the Ross Lab of the George Anne Ryan Institute for Neuroscience notes the concerning ability of MPs to penetrate the blood-brain barrier. This is especially alarming due to the brain's vulnerability to inflammation and oxidative stress, both of which are involved in Alzheimer’s pathology. While some inflammation was expected, researchers were surprised to find decreased levels of glial fibrillary acidic protein (GFAP), crucial for supporting brain cell processes activated in response to neural stress [9]. As Ka Young Kim highlights, increasing evidence suggests that low blood GFAP levels can indicate early-stage Alzheimer's [10]. The unexpected alteration in GFAP signaling due to MPs raises alarms about how these pollutants might disrupt normal brain processes, potentially contributing to cognitive decline.
Parkinson’s Disease
A November 2023 study co-authored by Arpine Sokratian and Zhiyong Liu Dr. Liu investigated how nanoplastics (NPs) can cross the blood-brain barrier to impact the progression of Parkinson's Disease (PD), a neurodegenerative disease that affects motor control [11]. The study found that NPs can bind to a protein called α-synuclein that contributes to PD pathology and accelerates its aggregation in nerve cells, leading to harmful buildup in brain regions affected by PD. The study found that NPs can bind to α-synuclein and accelerate its aggregation in nerve cells, leading to harmful buildup in brain regions affected by PD [11]. Another study led by Boxuan Liang investigated the effects of PS-NPs on PD using a mouse model [12]. The study involved 151 adult male mice who were exposed to different doses of PS-NPs (ranging from 0.25 to 250 mg per kg of body weight) every day for 28 days. The researchers found that even low doses of PS-NPs were able to enter the brain and accumulate in areas usually affected by PD, such as the substantia nigra and striatum areas of the brain. The exposed mice showed signs of motor problems, including reduced movement, weaker grip strength, and balance issues—symptoms that resemble those seen in humans with PD. Further investigation into the brain showed disruptions in energy use and protein functions, which are important for brain health and are known to be affected in PD [12]. These results suggest that exposure to NPs could contribute to the development or worsening of PD, adding to growing concerns about the potential health risks of plastic pollution, particularly its impact on the brain.
Demyelination
Myelin is the protective sheath that surrounds nerve fibers, facilitating efficient communication between neurons. Complementing this research, a study led by Yaping Zhang examined the effects of NPs on myelin formation in the cerebellum, an area of the brain crucial for motor control and coordination [13]. In the study, researchers administered NPs to pregnant rats and then analyzed the brains of their offspring to assess levels of key proteins involved in myelin formation. Protein measurements showed significant changes in these myelin formation proteins. Notably, the cerebellum emerged as a primary site for NP accumulation, raising concerns about its impact on brain development. The study revealed a marked decrease in two important proteins: myelin basic protein and myelin oligodendrocyte glycoprotein, both of which are essential for maintaining myelin integrity. The brain contains crucial lipid-rich areas like myelin sheaths; disruption of myelin integrity can compromise signaling between neurons, which may lead to various neurological disorders, including ataxia (loss of coordination), multiple sclerosis, and Alzheimer’s disease. Changes in myelination can affect the support provided by oligodendrocytes, which are cells that create myelin, alter nerve conduction speed, and ultimately reshape neural circuits during critical stages of development [13]. These connections highlight the urgent need for more research into the long-term effects of microplastics on neurological health, especially given the increasing prevalence of Alzheimer’s and related dementias.
Epidemiological Concerns and Recommendations
The studied presence of MNPs in human brain tissue raises significant epidemiological concerns regarding their potential impact on neurological health, warranting urgent action. MPs are pervasive in the environment—found in air, water, and food—resulting in widespread exposure across various demographics, making this issue a pressing public health concern. Certain populations, particularly individuals with preexisting health conditions, may be more susceptible to the neurotoxic effects of plastics. As MNP research progresses, there is a pressing need to identify these vulnerabilities to allow for targeted public health interventions. Furthermore, there is a noticeable and critical gap in longitudinal studies that examine the long-term effects of MP exposure on overall human brain health and function. Without this data, establishing causation and fully understanding the implications of MNPs for collective public health remains challenging. The accumulating evidence of MPs in brain tissue should call for stricter regulations on plastic production and waste management, as well as enhanced public health campaigns to raise awareness about reducing plastic consumption in a way that minimizes catastrophic reactions. As Vethaak and Legler highlight, it is crucial to understand the contribution of MPs to total ambient particle exposure and evaluate their potential impact on global disease burdens [14]. Addressing these issues proactively will potentially mitigate the long-term health effects associated with MNP exposure and protect future generations.

As highlighted by recent studies, the mechanisms by which MNPs infiltrate the brain and contribute to conditions like Alzheimer’s disease warrant significant concern. Moreover, the epidemiological implications of MP exposure, particularly for vulnerable populations, call for targeted public health interventions and policy reforms aimed at reducing plastic consumption and improving waste management. While it is crucial to stay informed about the scientific findings surrounding MPs, we should avoid becoming overwhelmed by the notion of completely eliminating them from our bodies. As Wu notes, research on MPs is still in its early stages, and further investigations are essential to fully understand their environmental occurrences and impacts [15]. Moving forward, a balanced approach that combines awareness, research, and proactive measures will be vital in addressing the challenges posed by plastics. For now, increasing importance lies in staying mindful of the impacts of healthier food choices, general plastic consumption, and industrial pollution that contribute to neurological health and well-being.
References
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