Early-life exposure to polypropylene microplastics and DEHP induces ASD-relevant neurodevelopmental alterations involving mTOR-regulated autophagy impairment
What this study shows
PP-MPs and DEHP activate mTOR and impair autophagy, inducing ASD-like neurodevelopmental deficits in mice; rapamycin rescues autophagic flux and social/behavioral phenotypes.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Mouse (ICR, early-life exposure model)); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Mouse (ICR, early-life exposure model) |
| Journal | Ecotoxicology and Environmental Safety |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1016/j.ecoenv.2026.120659 · PMID 42600301 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Polypropylene microplastics (PP-MPs); DEHP; Rapamycin (rescue) |
| Target | mTOR signaling; autophagy; Shank3; Nlgn1 (synaptic plasticity) |
| Model | Mouse |
| Effect | mTOR hyperactivation + autophagy impairment mediates ASD-like neurotoxicity from early-life plastic/plasticizer exposure; mTOR inhibition is protective |
In the Atlas
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