| Species | MNPs types | Size | Method of administration | Exposure dose | Exposure duration | Neurotoxic effects | Ref |
|---|---|---|---|---|---|---|---|
| Male wistar rats (6~8 weeks) | PS-NPs | 25 and 50 nm | Oral gavage | 1，3，6，and 10 mg/(kg·d) | 35 d | No significant neurobehavioral effects. | Rafiee et al. [ |
| Male BALB/c mice (6 weeks) | PS-MPs | 0.5，4 and 10 μm | Drinking water exposure | 100 and 1000 μg/L | 180 d | Cognitive and memory deficits; disruption of the blood-brain barrier; reduced dendritic spine density; an inflammatory response in the hippocampus; a concentration-dependent trend. | Jin et al. [ |
| Male C57BL/6 mice (5 weeks) | PS-NPs | 25 nm | Oral gavage | 0，10，25， 50 mg/(kg·d) | 180 d | Cognitive decline; synaptic damage in the prefrontal cortex; increased sensitivity to synaptic dysfunction. | Chen et al. [ |
| Male C57BL/6 mice (5 weeks) | PS-NPs | 80 nm | Oral gavage | 60 μg/day | 42 d | Caused neuronal damage in the hippocampus，impaired learning and memory abilities; neurotoxicity involved gut-brain axis-mediated pathways related to circadian rhythm. | Kang et al. [ |
| Male C57BL/6 mice (7 weeks) | PS-NPs | 30~50 nm | Oral gavage | 10 and 20 mg/(kg·d) | 42 d | Induced memory impairment，activated microglia，triggered inflammatory responses，and dysregulated hippocampal neuronal activity. | Paing et al. [ |
| Male Swiss mice (4~6 weeks) | PS-NPs | 25 nm | Intraperitoneal administration | 14.6 ng/(kg·d) | 3 d | Cognitive impairment; REDOX imbalance; suppressed AChE activity; DNA damage. | Estrela et al. [ |
| Male or female C57BL/6 mice (6 weeks) | PS-MPs | 2 μm | Oral gavage | 8 and 16 mg/(kg·d) | 28 and 56 d | Learning and memory deficits; decreased synaptic protein levels; induced neuroinflammation. | Lee et al. [ |
| SH-SY5Y cells | Amine-functionaliz- ed PS-NPs | 50 nm | In culture medium | 1, 5, 10, and 50 µg/cm2 | 24 h and 48 h | Decreased neuronal differentiation and increased Amyloid β secretion. | Schroter et al. [ |
| SHSY-5Y cells | Unmodified and amino-modified PS-NPs | 70 and 150 nm | In culture medium | 100 pM | 24 h and 7 d | Accelerated the aggregation of β-amyloid peptides. | Gou et al. [ |
| Male C57BL/6 mice (6~8 weeks) | PS-MPs and PS-NPs | 100 nm and 1.0 µm | Oral gavage | 0.5 mg/day | 30 and 60 d | Induced anxiety-like behaviors; changed serum metabolic profiles，particularly in neurotransmitter metabolites. | Chen et al. [ |
| Male C57BL/6 mice (8 weeks) | PS-MPs | 480 nm | Oral gavage | 2 and 10 mg/(kg·d) | 180 d | Induced anxiety-like behavior; related to inflammation pathways. | Li et al. [ |
| Male C57BL/6 mice (5 weeks) | PS-NPs | 25 nm | Oral gavage | 10, 25 and 50 mg/(kg·d) | 180 d | Depression-like responses; activation of axon guidance，the neurotrophin signaling pathway，and dopaminergic synapse-related lncRNAs. | Liu et al. [ |
| Male BALB/c mice (4 weeks) | PS-NPs with different surface modifications (PS，PS-COOH，and PS-NH2) | ∼100 nm | Oral gavage | 1 mg/day | 28 d | Disrupted the tight junctions formed by brain endothelial cells; induced mitochondrial dysfunction in neurons; induced anxiety，depression，and social deficits. | Ma et al. [ |
| Male Swiss albino mice (10 weeks) | PS-NPs | 50 nm | Oral gavage | 0.2 and 1 mg/(kg·d) | 56 d | Induced anxiogenic behavior and impaired learning; induced oxidative stress and inhibited acetylcholinesterase activity; decreased the number of hippocampal pyramidal cells; affected neuronal architecture of the cortex and hippocampus. | Sharma et al. [ |
| Male C57BL/6 mice (8 weeks) | PS-NPs | 50 nm | Oral gavage | 0.5, 5, 50 and 500 mg/(kg·d) | 28 d | Induced Parkinson’s disease (PD)-like neurodegeneration; disturbed PD-associated gene expression; inhibited ATP metabolism | Liang et al. [ |
| Male C57BL/6 mice (8 weeks) and SHSY-5Y cells | PS-NPs | 50 nm | in vivo:Oral gavag; in vitro: in culture medium | in vivo: 500 mg/(kg·d) ; in vitro: 0.25，2.5, 25, 250 μg/mL | in vivo: 28 d in vitro: 48 h | PS-NPs disrupted mitochondrial function by affecting CI，leading to excessive mitophagy through the AMPK/ULK1 pathway，ultimately causing dopaminergic neuron death. | Huang et al. [ |
| Primary neuron; CD1 mice (3 months) | Anionic and cationic PS-NPs | 23.2~ 115.6 nm | in vivo: intracranial injection; in vitro: in culture medium | in vivo: 15 μg; in vitro: 1 nM | in vivo: 3-d, or two months; in vitro: 24 h | Causing mild lysosomal impairment that slows the degradation of aggregated α-synuclein; exacerbates the spread of α-synuclein pathology across interconnected vulnerable brain regions. | Liu et al. [ |
| C. elegans strains; A53T α-syn-EGFP SH-SY5Y cells | PS-NPs | 25 nm | in vivo: in culture medium; in vitro: in culture medium | in vivo: 10，100，or 1000 μg/L; in vitro: 15 mg/L | in vivo: 24 h; in vitro: 24 h | Low concentrations of nanoplastics inhibit the growth and movement of nematodes; increase α-synuclein aggregation. | Jeong et al. [ |
| SD pregnant rats | PS-NPs | 25 and 50 nm | Oral gavage | 0.5, 2.5, 10 and 50 mg/(kg·d) | 1st to the 18th day of pregnancy | Affect the growth and development of fetal rats; damage the placental barrier; cause oxidative stress and inflammatory responses. | Zhang et al. [ |
| Pregnant female C57BL/6 mice | PS-NPs | 50 and 500 nm | Oral administration | 0.5~1000 μg/day | embryonic day 8 until 2 weeks after birth | Induced neurodevelopmental defects; caused NSC dysfunction; led to the dysregulation of brain functions in progeny. | Jeong et al. [ |
| 3D model of human forebrain cortical spheroids | PS-MPs | 1 and 10 μm | In culture medium | 5，50，and 100 µg/mL | 6 and 26 d | Altered the gene expression related to DNA damage and neural tissue patterning; affected embryonic brain-like tissue development in forebrain cerebral spheroids. | Hua et al. [ |
| C57BL/6 J mice (8-weeks) | PS-MPs | 2 μm | Drinking water exposure | 1 mg/L | embryonic stage to adulthood | Impaired offspring social novelty preferences. | So et al. [ |
| Female C57BL/6 J mice | PE-MPs | 10~20 μm | Oral gavage | 10 μg/day | prenatal: 14 d; post-weaning period: 14 d; puberty: 14 d; adult: 84 d. | Impaired social interaction and repetitive behaviors; disturbance of metabolites and gene expression in the brain; leads to Autism Spectrum Disorder (ASD)-like traits. | Zaheer et al. [ |
| Male C57BL/6 mice (8 weeks); hCMEC/D3，murine microglia BV2，hippocampus-derived neuronal HT22 cells | PS-NPs | 42 nm | in vivo: Oral gavage; in vitro: in culture medium | in vivo: 0.5，2.5，10，and 50 mg/(kg·d); in vitro: 0，25，50，and 100 μg/mL | in vivo: 7 d; in vitro: 48 h | Induced microglia activation and neuronal damage in the brain; caused oxidative stress，inflammatory response，and necroptosis in hCMEC/D3 cells; disrupted tight junctions. | Shan et al. [ |
| Male C57BL/6 mice (3 weeks) | PS-MPs | 5 and 50 μm | Drinking water exposure | 100 and 1000 μg/L | 70 d | Induced social disorders in adult mice; decreased oxytocin levels; reduced mucin layers and caused gut microbiota dysbiosis. | Wang et al. [ |
| Male Swiss albino mice (20~30 g) | PS-MPs | 500 nm | Oral gavage | 0.1，1，and 10 ppm | 28 d | Reduced Nissl bodies in the PFC; affected neuronal cytoarchitecture of PFC neurons; decreased spine density in PFC neurons; down-regulated BDNF gene. | Suman et al. [ |
| Male KM mice (5 weeks) | PS-MPs | 5.0~5.9 μm | Oral gavage | 1 mg/d | 28 d | Impaired learning and memory functions; induced a reduction in the level of acetylcholine; increased levels of ROS and MDA. | Wang et al. [ |
| KM mice (18~22 g); NS20Y cells | PS-MPs; Di-(2-ethylhexyl) phthalate (DHEP) | 1~10 μm | Food and water exposure | in vivo: food containing 200 mg/kg DEHP and water containing 10 mg/L MPs; in vitro: 25 μmol/L DEHP and 775 mg/L PS-MPs | in vivo: 30 d; in vitro: 24 h | DEHP and MPs caused changes in mitochondrial function; led to apoptosis of neurons; exhibited a combined toxic effect on mouse cerebra. | Zhang et al. [ |
| Male ICR mice (3 weeks) | PP-MPs; DHEP | / | Oral gavage | PP-MPs: 5，20 and 80 mg/(kg·d); DHEP: 250 mg/(kg·d) | 28 d | Neurocognitive defects; induced impairments in the hippocampal CA3 region; exhibited additive or synergistic toxic effects. | Yang et al. [ |
| Male C57BL/6 mice (7~8 weeks) | PS-MPs; doxycycline hyclate (Dox) | 500 nm | Oral gavage | PS-MPs: 5 mg/(kg·d); Dox: 20 mg/(kg·d) | 30 d | Co-exposure caused brain lesions and inflammation; decreased learning and memory behaviors through the gut-brain axis. | Sun et al. [ |
| Male C57BL/6 mice (9 months) | PS-MPs; Ferric ammonium citrate (FAC) | 5 µm | Drinking water exposure | PS-MPs: 1000 μg/L; Dox: 5 g/L | 90 d | Co-exposure caused significant iron overload and cognitive deficits; elevated lipid peroxidation and inflammation; aggravated cognitive impairment. | Liu et al. [ |
