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61,005 resultsShowing papers similar to Microplastic Exposure Promotes Amyloid Misfolding and Metabolic Impairment at Sub-Lethal Doses in an In Vitro Cellular Model of Alzheimer’s Disease
ClearImpact of nanoplastics on Alzheimer ’s disease: Enhanced amyloid-β peptide aggregation and augmented neurotoxicity
Researchers found that even very low concentrations of polystyrene nanoplastics can speed up the clumping of amyloid-beta protein, a hallmark of Alzheimer's disease, and increase its toxicity to brain cells. The hydrophobic (water-repelling) surface of the nanoplastics helps the proteins stick together faster, suggesting a potential link between environmental nanoplastic exposure and increased risk of Alzheimer's disease.
Short-Term Exposure to Polystyrene Microplastics Alters Cognition, Immune, and Metabolic Markers in an APOE Genotype and Sex-Dependent Manner
Researchers exposed Alzheimer's disease mouse models to polystyrene microplastics for a short term and observed worsened cognitive performance, altered immune markers, and disrupted metabolic pathways, suggesting that MP exposure may accelerate neurological decline in individuals already vulnerable to dementia.
Microglial clearance of Alzheimer's amyloid-beta obstructed by nanoplastics
Researchers found that polystyrene nanoplastics interfere with the brain's ability to clear amyloid-beta, the protein that builds up in Alzheimer's disease. The nanoplastics accelerated amyloid clumping and drained the energy of brain immune cells that normally clean up these harmful proteins. This study suggests that nanoplastic exposure could worsen or contribute to the development of Alzheimer's disease.
Food-borne polystyrene microplastic exposure exacerbates cognitive deficiency via enhanced neuronal synaptic damage and neuroinflammation in Alzheimer's disease
This study exposed Alzheimer's disease model mice (APP/PS1) to polystyrene microplastics via food and found that MP exposure worsened cognitive deficits by exacerbating hippocampal mitochondrial damage and neuroinflammation. The results suggest MP exposure may accelerate Alzheimer's disease progression in vulnerable individuals.
Exposure to Polystyrene Microplastics Promotes the Progression of Cognitive Impairment in Alzheimer’s Disease: Association with Induction of Microglial Pyroptosis
In a mouse study, polystyrene microplastics worsened cognitive decline in an Alzheimer's disease model by triggering a type of inflammatory cell death called pyroptosis in brain immune cells. The microplastics caused brain inflammation that accelerated memory loss and cognitive impairment beyond what Alzheimer's alone caused. This is one of the first studies suggesting that microplastic exposure could make neurodegenerative diseases like Alzheimer's progress faster.
Cerebral to SystemicRepresentations of Alzheimer’sPathogenesis Stimulated by Polystyrene Nanoplastics
Researchers exposed both wild-type and APP/PS1 Alzheimer's model mice to environmental levels of polystyrene nanoplastics and measured Alzheimer's-like pathology progression. Nanoplastics exacerbated cognitive decline, microglial activation, and hippocampal neuronal death, particularly in the Alzheimer's model, with systemic inflammatory effects suggesting plastic particles may accelerate neurodegeneration.
Nanoplastics exposure exacerbates Aβ plaque deposition in Alzheimer’s disease mice by inducing microglia pyroptosis
In Alzheimer's disease model mice, exposure to environmentally relevant doses of nanoplastics worsened cognitive problems and increased the brain plaques associated with the disease. The nanoplastics damaged a waste-clearing system in brain immune cells called microglia, reducing their ability to remove harmful amyloid plaques, though the study also found that melatonin treatment helped restore brain cell function and reduce plaque buildup.
Cerebral to Systemic Representations of Alzheimer’s Pathogenesis Stimulated by Polystyrene Nanoplastics
Researchers found that environmentally realistic levels of polystyrene nanoplastics worsened Alzheimer's disease symptoms in mice, triggering brain inflammation, neuron death, and cognitive decline. The nanoplastics also disrupted metabolism and caused organ damage beyond the brain, including liver and kidney effects. This study provides some of the first evidence that nanoplastic exposure could accelerate brain diseases like Alzheimer's, especially as nanoplastics have been found in human brain tissue.
DMSP for 'Quantitative Assessment of Nanoplastics in Alzheimer's Disease Brain and Their Role in Amyloid-β Aggregation'
Researchers quantitatively assessed nanoplastic contamination in Alzheimer's disease brain tissue and investigated whether nanoplastics play a role in amyloid-beta aggregation. The study suggests that nanoplastics, now ubiquitous in the environment and present in drinking water and food, may represent an environmental factor that could modify Alzheimer's disease pathology by interacting with amyloid-beta protein aggregation.
Evidence for protein misfolding in the presence of nanoplastics
Computer simulations suggest that nanoplastics — tiny plastic particles under 5 nanometers — can cause proteins to misfold when they bind together. Misfolded proteins are linked to diseases like Alzheimer's, making this an early warning that nanoplastics may pose risks at the molecular level in living cells.
Alzheimer’s disease: the role of extrinsic factors in its development, an investigation of the environmental enigma
This review examines how environmental contaminants, including microplastics, may contribute to Alzheimer's disease risk. Along with air pollutants, toxic metals, and pesticides, plastics and microplastics are identified as potential risk factors that may promote brain inflammation and neurodegeneration. The review explores the molecular mechanisms behind these effects and suggests strategies to reduce the brain health impacts of environmental contaminants.
Insights into the Binding Interactions between Microplastics and Human α-Synuclein Protein by Multispectroscopic Investigations and Amyloidogenic Oligomer Formation
Researchers found that common microplastics -- especially polystyrene -- can bind to alpha-synuclein, a brain protein whose clumping is a hallmark of Parkinson's disease. The microplastics altered the protein's structure and promoted the formation of toxic clumps called amyloidogenic oligomers. This suggests that microplastic exposure could potentially accelerate the protein misfolding process linked to Parkinson's and other neurodegenerative diseases.
The Effect of Polyethylene Terephthalate Nanoplastics on Amyloid-β Peptide Fibrillation
Lab experiments showed that PET nanoplastics, the type found in plastic bottles and clothing, accelerated the clumping of amyloid-beta proteins, which is a hallmark of Alzheimer's disease. Smaller nanoplastics (50 nm) had a stronger effect than larger ones, cutting the time for protein clumping nearly in half. While this is a test-tube study, it raises the question of whether nanoplastics that reach the brain could potentially speed up the development of Alzheimer's-related protein buildup.
Elucidating the Neurotoxicopathological Impact of Micro and Nanoplastics: Mechanistic Insights Into Oxidative Stress-mediated Neurodegeneration and Implications for Public Health in a Plastic Pervasive Era
Researchers reviewed the growing evidence linking micro- and nanoplastic exposure to neurodegenerative diseases, identifying oxidative stress, neuroinflammation, DNA damage, and protein misfolding as key mechanisms of harm to the brain. The review highlights critical knowledge gaps — especially around chronic low-dose exposure — and calls for better detection tools and public health policies to address the emerging neurological threat from plastic pollution.
A novel risk factor for dementia: chronic microplastic exposure
This review examines emerging evidence that chronic microplastic exposure may be a previously overlooked risk factor for dementia. Microplastics can cross the blood-brain barrier and may promote brain damage through oxidative stress, inflammation, and by accelerating the buildup of amyloid plaques linked to Alzheimer's disease, with studies finding higher microplastic levels in the brains of dementia patients compared to controls.
Effects of Microplastic Accumulation on Neuronal Death After Global Cerebral Ischemia
Researchers found that microplastics worsened brain damage after a stroke-like event in mice, increasing inflammation, damaging the protective coating around nerve fibers, and causing more brain cell death. The microplastics also triggered the release of abnormal tau proteins, similar to what happens in Alzheimer's disease, suggesting that microplastic exposure could make the brain more vulnerable to injury and neurodegenerative conditions.
Microplastic exposure linked to accelerated aging and impaired adipogenesis in fat cells
Researchers found that microplastic exposure accelerates aging in fat tissue by triggering cellular senescence (a state where cells stop dividing and release inflammatory signals) in both mice and cell cultures. The microplastics accumulated in fat tissue, increased markers of aging and inflammation, and disrupted the normal development of new fat cells. These findings suggest that chronic microplastic exposure could contribute to age-related metabolic problems and obesity-related diseases in humans.
Plastic Nanoparticles Cause Proteome Stress and Aggregation by Compromising Cellular Protein Homeostasis ex vivo and in vivo.
Researchers demonstrated for the first time that plastic nanoparticles can compromise cellular protein homeostasis ex vivo and in vivo, causing proteome stress and protein aggregation by disrupting the cellular machinery responsible for maintaining protein stability. The findings suggest that nanoplastic exposure poses risks beyond cytotoxicity, potentially triggering protein misfolding pathways relevant to neurodegenerative and other protein aggregation diseases.
The Role of Emerging Environmental Contaminants on Alzheimer’s Disease
This review examined the role of emerging environmental contaminants, including microplastics, in the development and progression of Alzheimer's disease. The authors discussed mechanisms including oxidative stress, neuroinflammation, and blood-brain barrier disruption as potential pathways linking environmental exposures to AD pathogenesis.
Alzheimer's Disease: New Perspectives
This review of Alzheimer's disease research challenges the dominant amyloid hypothesis and examines evidence that toxic environmental exposures — including microplastics and their chemical additives — may contribute to disease risk, arguing for broader investigation of environmental factors in neurodegeneration.
The Effect of Polyethylene Terephthalate Nanoplastics on Amyloid-β Peptide Fibrillation
Researchers investigated whether PET nanoplastics (50 nm and 140 nm) affect the fibrillation of amyloid-beta peptides associated with Alzheimer's disease pathology. PET nanoplastics at concentrations of 10–100 ppm influenced Aβ aggregation kinetics in a size- and concentration-dependent manner, adding to evidence that nanoplastics reaching the brain may modulate neurodegenerative protein aggregation.
Gradual effects of gradient concentrations of polystyrene nanoplastics on metabolic processes of the razor clams
Researchers exposed razor clams to a gradient of polystyrene nanoplastic concentrations and used metabolomics to track effects, finding that even low concentrations disrupted energy metabolism and amino acid pathways, with effects becoming more severe as concentration increased.
Low-Density Polyethylene Microplastics in the Blood Seems not Induce Alzheimer’s Disease in Wistar Rat
Researchers investigated whether low-density polyethylene microplastics in the blood trigger Alzheimer's disease in Wistar rats, noting that these particles enter the human body through contaminated food sources including table salt, fish, tea bags, and drinking water.
Micro- and Nanoplastics’ Effects on Protein Folding and Amyloidosis
This review examines how micro- and nanoplastic particles may interact with proteins in the body, potentially influencing protein folding and triggering the formation of abnormal amyloid structures. The study suggests that plastic particles can cross the blood-brain barrier in animal models and interact with neurons, raising questions about possible links between plastic exposure and protein misfolding conditions.