Researchers highlight five pathways through which microplastics can harm the brain

Microplastics could be fueling 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.

“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.”

Kamal Dua, Associate Professor, University of Technology Sydney

“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.