Do Nanoplastics Speed Up Alzheimer’s Disease?

nanoplastics on fingertips

Experts have revealed undeniable health hazards associated with microplastics, tiny plastic fragments that fail to break down in the environment. Now, experts are assessing the risks associated with nanoplastics: plastic particles even smaller than microplastics, measuring between one and 1,000 nanometers in size. These microscopic fragments are highly prevalent in the environment and can easily penetrate cells and tissues thanks to their tiny size. In other words, nanoplastics are an even more concerning threat.

A new preclinical study, co-led by Monash University and South China University of Technology, examined the effects of nanoplastic on APP/PS1 mouse models of Alzheimer’s disease (AD). The study found that exposure to nanoplastics may contribute to the rapid progression of AD, accelerating its effects throughout the body.

Read on for a summary of the research, “Cerebral to Systemic Representations of Alzheimer’s Pathogenesis Stimulated by Polystyrene Nanoplastics,” which was published July 22 in the journal Environment & Health.

Nanoplastics: Tiny, Ubiquitous, and Harmful

Humans are exposed to plastics every day through a combination of inhalation, physical contact, and contaminated food and water. While these plastics are tiny, the medical community is only beginning to grasp their potentially harmful effects. In fact, the researchers behind the July 22 study called nanoplastics “a threat to environmental sustainability and human health,” pointing out that nanoplastics have been identified “in abundance in the human brain.” Oddly, this is especially true when evaluating the brain tissues of individuals with dementia.

Is there a connection between environmental-level nanoplastic exposure and the progression of AD? The research says yes.

Evaluating Nanoplastics’ Impact on APP/PS1 Mice

To evaluate the dangers of nanoplastics, the Monash-South China University researchers used both wild type and APP/PS1 double transgenic mice. This mouse model provides an effective model of AD characterized by elevated β-amyloid production and behavioral abnormalities.

The mice were divided into four groups: wild type control mice injected with saline, wild type mice injected with a water suspension of polystyrene (PS) nanoplastics, APP/PS1 control mice, and APP/PS1 mice injected with PS nanoplastics. All injections were performed intracerebroventricularly. The mice were then tested using the Morris water maze test, a common behavioral test for rodent spatial learning and memory.

Morris Water Maze Test Reveals Significant Impact

Ultimately, the PS nanoplastics aggravated AD-like symptoms in both wild type and APP/PS1 mice, as shown during the Morris water maze test. The nanoplastics also had a stunning effect on the cellular level. The nanoplastics appeared to stimulate microglial activation and hippocampal neuronal death, and the mice also exhibited full-body symptoms, including hepatic steatosis and gut microbiota imbalance. The nanoplastics seemed to spur the effects of AD through other key organs, setting off a chain reaction of sorts.

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These data supplement previous nanoplastic studies in mice, which have shown that neurological damage expands systemically through the gut–liver–brain axis. Lead author of the study, Professor Pu Chun Ke, noted that the findings further support evidence that nanoplastics are a threat to human health. “These findings, although still early stage, suggest that nanoplastic-induced neurological damage is not confined within the brain but expands systemically through the communication network connecting the gastrointestinal tract, liver, and central nervous system,” Ke said. He added that future research should investigate different nanoplastic variants to aid “the development of preventive strategies for environmentally induced neurological disorders.”

To study AD in vivo, Scantox Neuro offers research with the 5xFAD mouse model that bears five AD-linked mutations: three in the APP695 gene and two more mutations in the PSEN1 gene. Animals can be injected and treated by different routes, and cognitive deficits can be evaluated by various behavioral tests. Several biochemical and histological techniques can be used to analyze AD-related brain pathology. Furthermore, various in vitro models of AD are readily available. Please contact us to discuss how Scantox Neuro can support your preclinical AD research.

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