Summary: A new review highlights five main ways microplastics can damage the brain, raising concerns that they could worsen neurodegenerative diseases such as Alzheimer’s and Parkinson’s. These small particles can trigger inflammation, disrupt the blood-brain barrier, generate oxidative stress, damage mitochondria, and damage neurons.
Evidence shows that microplastics accumulate in brain tissue, where they interact with disease pathways such as beta-amyloid, tau and α-synuclein. While more research is needed to confirm direct causality, reducing exposure to microplastics may help reduce long-term neurological risk.
Key facts
Five pathways of damage: Microplastics can trigger immune activation, oxidative stress, barrier disruption, mitochondrial damage and neuronal injury. Brain accumulation: Studies show that microplastics can enter and persist in the brain despite elimination mechanisms. Disease relevance: These effects align with the processes involved in the progression of Alzheimer’s and Parkinson’s.
Source: University of Technology Sydney
Microplastics could be fueling neurodegenerative diseases like Alzheimer’s and Parkinson’s, and a new study highlights five ways microplastics can trigger inflammation and damage in the brain.
More than 57 million people live with dementia and cases of Alzheimer’s and Parkinson’s are expected to increase significantly. The possibility that microplastics could aggravate or accelerate these brain diseases is a major public health concern.
Pharmaceutical scientist Associate Professor Kamal Dua, from the University of Technology Sydney, said adults are estimated to consume 250 grams of microplastics each year, enough to cover a plate.
“We ingest microplastics from a wide range of sources, including contaminated seafood, salt, processed foods, tea bags, plastic cutting boards, drinks in plastic bottles and foods grown in contaminated soil, as well as plastic fibers from carpets, dust and synthetic clothing.”
“Common plastics include polyethylene, polypropylene, polystyrene and polyethylene terephthalate or PET. Most of these microplastics are eliminated from our body, however, studies show that they accumulate in our organs, including the brain.”
The systematic review, recently published in Molecular and Cellular Biochemistry, was an international collaboration led by researchers from the University of Technology Sydney and Auburn University in the United States.
The researchers highlighted five main pathways through which microplastics can cause damage to the brain, including triggering immune cell activity, generating oxidative stress, disrupting the blood-brain barrier, impairing mitochondria, and damaging neurons.
“Microplastics actually weaken the blood-brain barrier, making it permeable. Once this happens, immune cells and inflammatory molecules are activated, causing even more damage to the barrier cells,” said Associate Professor Dua.
“The body treats microplastics as foreign intruders, causing immune cells in the brain to attack them. When the brain is stressed by factors such as toxins or environmental pollutants, this also causes oxidative stress,” he said.
Microplastics cause oxidative stress in two main ways: they increase the amount of “reactive oxygen species,” or unstable molecules that can damage cells, and they weaken the body’s antioxidant systems, which normally help keep those molecules in check.
“Microplastics also interfere with the way mitochondria produce energy, reducing the supply of ATP or adenosine triphosphate, which is the fuel cells need to function. This energy deficit weakens neuronal activity and can ultimately damage brain cells,” said Associate Professor Dua.
“All of these pathways interact with each other to increase damage in the brain.”
The article also explores specific ways in which microplastics could contribute to Alzheimer’s, including increasing the accumulation of beta-amyloid and tau; and in Parkinson’s through the aggregation of α-synuclein and damage to dopaminergic neurons.
First author Alexander Chi Wang Siu, a UTS Master of Pharmacy student, is currently working in Professor Murali Dhanasekaran’s laboratory at Auburn University, in collaboration with co-authors Associate Professor Dua, Dr Keshav Raj Paudel and UTS Distinguished Professor Brian Oliver, to better understand how microplastics affect brain cell function.
Previous UTS research has examined how microplastics are inhaled and where they are deposited in the lungs. Dr Paudel, a visiting academic at the UTS Faculty of Engineering, is also currently researching the impact of inhaling microplastics on lung health.
While evidence suggests that microplastics could worsen diseases such as Alzheimer’s and Parkinson’s, the authors emphasize that more research is needed to demonstrate a direct link. However, they recommend taking measures to reduce exposure to microplastics.
“We need to change our habits and use less plastic. Stay away from plastic containers and cutting boards, don’t use the dryer, choose natural fibers instead of synthetic ones, and eat less processed and packaged foods,” Dr. Paudel said.
Researchers hope the current findings will help shape environmental policies to reduce plastic production, improve waste management, and reduce the long-term public health risks posed by this ubiquitous environmental pollutant.
Key questions answered:
A: Microplastics can cross or weaken the blood-brain barrier, accumulate in neural tissue and trigger inflammatory and oxidative processes that damage brain cells.
A: Its effects overlap with known disease mechanisms, including beta-amyloid and tau accumulation in Alzheimer’s and α-synuclein aggregation and damage to dopaminergic neurons in Parkinson’s.
A: Limiting plastic containers, avoiding plastic cutting boards, choosing natural fibers, eating fewer processed foods, and reducing the use of dryers can help reduce consumption.
Editorial notes:
This article was edited by a Neuroscience News editor. Magazine article reviewed in its entirety. Additional context added by our staff.
About this news on research in microplastics and neurology
Author: Leilah Schubert
Source: University of Technology Sydney
Contact: Leilah Schubert – University of Technology Sydney
Image: Image is credited to Neuroscience News.
Original research: Open access.
“Do microplastics play a role in the pathogenesis of neurodegenerative diseases? Shared pathophysiological pathways for Alzheimer’s and Parkinson’s disease” by Kamal Dua et al. Molecular and cellular biology
Abstract
Do microplastics play a role in the pathogenesis of neurodegenerative diseases? Shared pathophysiological pathways for Alzheimer’s and Parkinson’s disease
The widespread presence of microplastics (MPs) in the environment has raised significant concerns about their potential impact on human health.
As of 2023, the Ocean Conservancy estimates that adults can ingest up to 121,000 MP annually. While the majority of these particles are eliminated from the body, a small fraction may persist, as MPs are non-biodegradable and resist degradation, posing long-term health risks that are not yet well understood.
This review explores the emerging link between MP exposure and the development of neurodegenerative diseases, particularly Alzheimer’s disease (AD) and Parkinson’s disease.
MPs appear capable of triggering neurotoxic pathways, including brain-resident immune cell activation, oxidative stress, blood-brain barrier (BBB) disruption, mitochondrial dysfunction, and neuronal damage, which may contribute to neuroinflammation and disease progression.
Specifically, six MP-related mechanistic pathways associated with AD were identified: BBB disruption, chronic inflammation, oxidative stress and ROS generation, mitochondrial dysfunction, impaired autophagy and proteostasis, and epigenetic alterations.
Similarly, six pathways were implicated in PD: disruption of the BBB, oxidative stress in dopaminergic neurons, mitochondrial dysfunction, microglial-driven neuroinflammation, α-synuclein aggregation, and disruption of the gut-brain axis.
Ultimately, our findings underscore the urgent need for more research into the neurological consequences of chronic PM exposure in humans and highlight the importance of strengthening global policies to curb plastic pollution and mitigate its long-term health risks.
