This shows a person drinking from a plastic water bottle and a brain.
All these pathways interact with each other to increase damage in the brain. Credit: Neuroscience News

Microplastics Accelerate Alzheimer’s and Parkinson’s Damage

Summary: A new review highlights five major ways microplastics can harm the brain, raising concerns that they may worsen neurodegenerative diseases like Alzheimer’s and Parkinson’s. These tiny particles can trigger inflammation, disrupt the blood–brain barrier, generate oxidative stress, impair mitochondria, and damage neurons.

Evidence shows 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 causation, reducing microplastic exposure may help lower long-term neurological risk.

Key Facts

  • Five Harm Pathways: Microplastics can trigger immune activation, oxidative stress, barrier disruption, mitochondrial damage, and neuron injury.
  • Brain Accumulation: Studies show microplastics can enter and persist in the brain despite clearance mechanisms.
  • Disease Relevance: These effects align with processes involved in Alzheimer’s and Parkinson’s progression.

Source: University of Technology Sydney

Microplastics could be fuelling neurodegenerative diseases like Alzheimer’s and Parkinson’s, with a new study highlighting 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 projected to rise sharply. 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 it is estimated that adults are consuming 250 grams of microplastics every year – enough to cover a dinner plate.

“We ingest microplastics from a wide range of sources including contaminated seafood, salt, processed foods, tea bags, plastic chopping boards, drinks in plastic bottles and food grown in contaminated soil, as well as plastic fibres from carpets, dust and synthetic clothing.”

“Common plastics include polyethylene, polypropylene, polystyrene and polyethylene terephthalate or PET. The majority of these microplastics are cleared from our bodies, however studies show they do accumulate in our organs, including our brains.”

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 US.

The researchers highlighted five main pathways through which microplastics can cause harm 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 leaky. Once that happens, immune cells and inflammatory molecules are activated, which then causes even more damage to the barrier’s cells,” said Associate Professor Dua.

“The body treats microplastics as foreign intruders, which prompts the brain’s immune cells to attack them. When the brain is stressed by factors like 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 shortfall weakens neuron activity and can ultimately damage brain cells,” said Associate Professor Dua.

“All these pathways interact with each other to increase damage in the brain.”

The paper also explores specific ways in which microplastics could contribute to Alzheimer’s, including triggering increased buildup of beta-amyloid and tau; and in Parkinson’s through aggregation of α-Synuclein and damage to dopaminergic neurons.

First author UTS Master of Pharmacy student Alexander Chi Wang Siu is a currently working in the lab of Professor Murali Dhanasekaran at Auburn University, in collaboration with co-authors Associate Professor Dua, Dr Keshav Raj Paudel and Distinguished Professor Brian Oliver from UTS, 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 scholar in the UTS Faculty of Engineering, is also currently investigating the impact of microplastic inhalation on lung health.

While evidence suggests microplastics could worsen diseases like Alzheimer’s and Parkinson’s, the authors emphasise that more research is needed to prove a direct link. However, they recommend taking steps to reduce microplastic exposure.

“We need to change our habits and use less plastic. Steer clear of plastic containers and plastic cutting boards, don’t use the dryer, choose natural fibres instead of synthetic ones and eat less processed and packaged foods,” said Dr Paudel.

The researchers hope the current findings will help shape environmental policies to cut plastic production, improve waste management and reduce long-term public health risks posed by this ubiquitous environmental pollutant.

Key Questions Answered:

Q: How can microplastics reach and affect the brain?

A: Microplastics can cross or weaken the blood–brain barrier, accumulate in neural tissue, and trigger inflammatory and oxidative processes that damage brain cells.

Q: Why might microplastics worsen Alzheimer’s or Parkinson’s?

A: Their effects overlap with known disease mechanisms, including beta-amyloid and tau buildup in Alzheimer’s and α-Synuclein aggregation and dopaminergic neuron injury in Parkinson’s.

Q: What steps can reduce microplastic exposure?

A: Limiting plastic containers, avoiding plastic cutting boards, choosing natural fibers, consuming fewer processed foods, and reducing dryer use can help lower intake.

Editorial Notes:

  • This article was edited by a Neuroscience News editor.
  • Journal paper reviewed in full.
  • Additional context added by our staff.

About this microplastics and neurology research news

Author: Leilah Schubert
Source: University of Technology Sydney
Contact: Leilah Schubert – University of Technology Sydney
Image: The 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 may ingest up to 121,000 MPs annually. While the majority of these particles are cleared from the body, a small fraction can persist, as MPs are non-biodegradable and resist breakdown, posing long-term health risks that remain poorly 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 activation of resident immune cells in the brain, 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: BBB disruption, oxidative stress in dopaminergic neurons, mitochondrial dysfunction, microglial-driven neuroinflammation, α-synuclein aggregation, and gut–brain axis disruption.

Ultimately, our findings underscore the urgent need for further research into the neurological consequences of chronic MP exposure in humans and highlight the importance of strengthening global policies to curb plastic pollution and mitigate its long-term health risks.

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