{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T03:53:13Z","timestamp":1782964393198,"version":"3.54.5"},"reference-count":50,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T00:00:00Z","timestamp":1774483200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Toxicol."],"abstract":"<jats:p>Neuroinflammatory contributions play a critical role in Parkinson\u2019s disease onset and progression. Key drivers of neuroinflammation include glial cell reactivity, cytokine signaling, protein aggregation, and mitochondrial dysfunction. Although animal models have been extensively used to investigate the mechanisms, their translational relevance is limited because neuroinflammation in humans is typically chronic, heterogeneous, and sustained over years, whereas in rodents is often acute, transient, and resolves within days to weeks. This paper highlights the utility of human stem cell\u2013derived models in studying Parkinson\u2019s disease by recapitulating patient-specific genetic mutations, neuroinflammatory microglia\u2013neuron interactions, \u03b1-synuclein aggregation, and dopaminergic dysfunction, thereby enabling mechanistic studies in the human-relevant models. In addition, we examine how micro- and nanoplastics may exacerbate neuroinflammation in PD. This review concludes by highlighting how human-relevant stem cell-based approaches advance mechanistic understanding of Parkinson\u2019s disease.<\/jats:p>","DOI":"10.3389\/ftox.2026.1723092","type":"journal-article","created":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T22:10:26Z","timestamp":1774476626000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Micro- and nanoplastics influences in Parkinson\u2019s disease: lessons from human stem cell models"],"prefix":"10.3389","volume":"8","author":[{"given":"Kamilah Na\u2019imah","family":"Muhammad","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, Brody School of Medicine, East Carolina University","place":["Greenville, NC, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tracey","family":"Woodlief","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, Brody School of Medicine, East Carolina University","place":["Greenville, NC, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xian","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, Brody School of Medicine, East Carolina University","place":["Greenville, NC, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,3,26]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"278","DOI":"10.1016\/j.neuron.2017.03.042","article-title":"iPSC-Derived human microglia-like cells to study neurological diseases","volume":"94","author":"Abud","year":"2017","journal-title":"Neuron"},{"key":"B2","doi-asserted-by":"publisher","first-page":"373","DOI":"10.3390\/brainsci11030373","article-title":"Modelling parkinson's disease: iPSCs towards better understanding of human pathology","volume":"11","author":"Avazzadeh","year":"2021","journal-title":"Brain Sci."},{"key":"B3","doi-asserted-by":"publisher","first-page":"792","DOI":"10.1007\/s12015-021-10254-3","article-title":"Human iPSC-Derived neural models for studying alzheimer\u2019s disease: from neural stem cells to cerebral organoids","volume":"18","author":"Barak","year":"2022","journal-title":"Stem Cell Rev. 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