Anionic nanoplastic contaminants promote Parkinson’s disease–associated α-synuclein aggregation
(2023) In Science Advances 9(46).- Abstract
Recent studies have identified increasing levels of nanoplastic pollution in the environment. Here, we find that anionic nanoplastic contaminants potently precipitate the formation and propagation of α-synuclein protein fibrils through a high-affinity interaction with the amphipathic and non-amyloid component (NAC) domains in α-synuclein. Nanoplastics can internalize in neurons through clathrin-dependent endocytosis, causing a mild lysosomal impairment that slows the degradation of aggregated α-synuclein. In mice, nanoplastics combine with α-synuclein fibrils to exacerbate the spread of α-synuclein pathology across interconnected vulnerable brain regions, including the strong induction of α-synuclein inclusions in dopaminergic neurons... (More)
Recent studies have identified increasing levels of nanoplastic pollution in the environment. Here, we find that anionic nanoplastic contaminants potently precipitate the formation and propagation of α-synuclein protein fibrils through a high-affinity interaction with the amphipathic and non-amyloid component (NAC) domains in α-synuclein. Nanoplastics can internalize in neurons through clathrin-dependent endocytosis, causing a mild lysosomal impairment that slows the degradation of aggregated α-synuclein. In mice, nanoplastics combine with α-synuclein fibrils to exacerbate the spread of α-synuclein pathology across interconnected vulnerable brain regions, including the strong induction of α-synuclein inclusions in dopaminergic neurons in the substantia nigra. These results highlight a potential link for further exploration between nanoplastic pollution and α-synuclein aggregation associated with Parkinson’s disease and related dementias.
(Less)
- author
- organization
- publishing date
- 2023-11
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Science Advances
- volume
- 9
- issue
- 46
- article number
- eadi8716
- publisher
- American Association for the Advancement of Science (AAAS)
- external identifiers
-
- pmid:37976362
- scopus:85177439091
- ISSN
- 2375-2548
- DOI
- 10.1126/sciadv.adi8716
- language
- English
- LU publication?
- yes
- id
- 771b5b02-0869-4d35-b6fb-ada6be0e52e8
- date added to LUP
- 2024-01-02 13:44:41
- date last changed
- 2024-09-19 03:22:22
@article{771b5b02-0869-4d35-b6fb-ada6be0e52e8, abstract = {{<p>Recent studies have identified increasing levels of nanoplastic pollution in the environment. Here, we find that anionic nanoplastic contaminants potently precipitate the formation and propagation of α-synuclein protein fibrils through a high-affinity interaction with the amphipathic and non-amyloid component (NAC) domains in α-synuclein. Nanoplastics can internalize in neurons through clathrin-dependent endocytosis, causing a mild lysosomal impairment that slows the degradation of aggregated α-synuclein. In mice, nanoplastics combine with α-synuclein fibrils to exacerbate the spread of α-synuclein pathology across interconnected vulnerable brain regions, including the strong induction of α-synuclein inclusions in dopaminergic neurons in the substantia nigra. These results highlight a potential link for further exploration between nanoplastic pollution and α-synuclein aggregation associated with Parkinson’s disease and related dementias.</p>}}, author = {{Zhiyong, Liu and Sokratian, Arpine and Duda, Addison M. and Xu, Enquan and Stanhope, Christina and Fu, Amber and Strader, Samuel and Li, Huizhong and Yuan, Yuan and Bobay, Benjamin G. and Sipe, Joana and Bai, Ketty and Lundgaard, Iben and Liu, Na and Hernandez, Belinda and Rickman, Catherine Bowes and Miller, Sara E. and West, Andrew B.}}, issn = {{2375-2548}}, language = {{eng}}, number = {{46}}, publisher = {{American Association for the Advancement of Science (AAAS)}}, series = {{Science Advances}}, title = {{Anionic nanoplastic contaminants promote Parkinson’s disease–associated α-synuclein aggregation}}, url = {{http://dx.doi.org/10.1126/sciadv.adi8716}}, doi = {{10.1126/sciadv.adi8716}}, volume = {{9}}, year = {{2023}}, }