We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Realistic-NPs trigger depression-like behaviors via mitochondrial iron overload mediating ferroptosis
AI summary Read the abstract
Researchers created environmentally realistic nanoplastics by mechanically fragmenting polystyrene and found that exposing mice to these particles induced depression-like behaviors within two weeks, along with later learning and memory deficits. The study identified mitochondrial iron overload and ferroptosis in the brain as the underlying mechanism, with the iron chelator deferoxamine able to reverse these effects.
ENVIRONMENTAL MICRO: and nanoplastics pose emerging neurotoxic risks, yet few studies have used environmentally realistic micro- and nanoplastics to elucidate underlying mechanisms. We prepared Realistic nano-polystyrene microplastics (Realistic-NPs) via mechanical fragmentation to mimic environmental plastics debris, characterized by irregular morphology and heterogeneous size distribution confirmed by FTIR and SEM analyses. Realistic-NPs exposure induced depressive-like behaviors in mice as early as 2 weeks, following spatial learning and memory deficits observed at 4 and 8 weeks. Histopathology revealed significant neuronal damage predominantly in prefrontal cortex, despite Realistic-NPs accumulated equally in prefrontal cortex and hippocampus. Mechanistically, Realistic-NPs triggered ferroptosis in above two brain regions, however, more pronounced iron overload, lipid peroxidation, and dysregulated ferroptosis markers were showed in prefrontal cortex. Treatment with the iron chelator deferoxamine mitigated these neurobehavioral and biochemical abnormalities. Realistic-NPs exposure induced mitochondrial iron overload in HT22 cells, which was mediated by upregulation of the mitochondrial iron importer MFRN2, and consequently contributed to mitochondrial dysfunction and ferroptosis. Integrative Mendelian randomization and single-cell transcriptomic data mining identified nuclear receptor coactivator 4 (NCOA4) as a central regulator linking ferroptosis to micro- and nanoplastics induced depressive-like behavior. Pharmacological inhibition of autophagy reduced ferroptosis induced by Realistic-NPs and improved neuronal survival. Collectively, our findings demonstrate that Realistic-NPs induce neurotoxicity through NCOA4-dependent ferritinophagy and ferroptosis mediated by mitochondrial iron overload, highlighting novel targets for therapeutic intervention against microplastic-induced neurological impairments.
More Papers Like This
Polystyrene nanoplastics induce hippocampal damage and cognitive deficits through oxidative stress-triggered microglial extracellular traps and neuronal ferroptosis
AI summary Read the abstract
Researchers showed that polystyrene nanoplastics impair spatial memory in mice by triggering a cascade in which hippocampal oxidative stress activates microglia to release extracellular traps, sustaining neuroinflammation that drives neuronal ferroptosis — a form of iron-dependent cell death — and that the antioxidant N-acetylcysteine blocks this entire pathway and preserves cognitive function.
Exposure to different surface-modified polystyrene nanoparticles caused anxiety, depression, and social deficit in mice via damaging mitochondria in neurons
AI summary Read the abstract
Mice exposed to polystyrene nanoplastics with different surface coatings all developed anxiety, depression, and impaired social behavior after the particles accumulated in their brains. The nanoplastics crossed the blood-brain barrier by disrupting the connections between blood vessel cells, then damaged the mitochondria (energy producers) inside brain neurons, reducing their energy output and likely driving the behavioral changes.
Co-exposure of polystyrene microplastics and iron aggravates cognitive decline in aging mice via ferroptosis induction
AI summary Read the abstract
Researchers studied the combined effects of microplastic and iron exposure on cognitive function in aging mice. They found that polystyrene microplastics accumulated in the brain's cortex and hippocampus, and when combined with iron, significantly worsened cognitive decline through a cell death process called ferroptosis. The study suggests that co-exposure to microplastics and metals may pose heightened risks to brain health in aging populations.
Unraveling the molecular pathways linking polystyrene exposure and depression
AI summary Read the abstract
This review examines experimental and epidemiological evidence linking polystyrene micro- and nanoplastic exposure to depression, tracing how these particles may cross the blood-brain barrier, accumulate in neural tissue, and trigger neuroinflammation, oxidative stress, mitochondrial dysfunction, and neurotransmitter disruption.
Polystyrene nanoplastics exposure induces cognitive impairment in mice via induction of oxidative stress and ERK/MAPK-mediated neuronal cuproptosis
AI summary Read the abstract
This mouse study found that polystyrene nanoplastics caused cognitive impairment by triggering oxidative stress and activating a cell-death process called cuproptosis in brain neurons. The findings suggest that copper buildup and specific signaling pathways may be therapeutic targets for reducing brain damage from nanoplastic exposure, though these results still need to be confirmed in human-relevant models.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.