Inflammation and α-Synuclein's Prion-like Behavior in Parkinson's Disease-Is There a Link?
(2013) In Molecular Neurobiology 47(2). p.561-574- Abstract
- Parkinson's disease patients exhibit progressive spreading of aggregated α-synuclein in the nervous system. This slow process follows a specific pattern in an inflamed tissue environment. Recent research suggests that prion-like mechanisms contribute to the propagation of α-synuclein pathology. Little is known about factors that might affect the prion-like behavior of misfolded α-synuclein. In this review, we suggest that neuroinflammation plays an important role. We discuss causes of inflammation in the olfactory bulb and gastrointestinal tract and how this may promote the initial misfolding and aggregation of α-synuclein, which might set in motion events that lead to Parkinson's disease neuropathology. We propose that neuroinflammation... (More)
- Parkinson's disease patients exhibit progressive spreading of aggregated α-synuclein in the nervous system. This slow process follows a specific pattern in an inflamed tissue environment. Recent research suggests that prion-like mechanisms contribute to the propagation of α-synuclein pathology. Little is known about factors that might affect the prion-like behavior of misfolded α-synuclein. In this review, we suggest that neuroinflammation plays an important role. We discuss causes of inflammation in the olfactory bulb and gastrointestinal tract and how this may promote the initial misfolding and aggregation of α-synuclein, which might set in motion events that lead to Parkinson's disease neuropathology. We propose that neuroinflammation promotes the prion-like behavior of α-synuclein and that novel anti-inflammatory therapies targeting this mechanism could slow disease progression. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2609345
- author
- Lema Tomé, Carla LU ; Tyson, Trevor LU ; Rey, Nolwen LU ; Grathwohl, Stefan ; Britschgi, Markus and Brundin, Patrik
- organization
- publishing date
- 2013
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Molecular Neurobiology
- volume
- 47
- issue
- 2
- pages
- 561 - 574
- publisher
- Humana Press
- external identifiers
-
- wos:000316120900011
- pmid:22544647
- pmid:22544647
- scopus:84888394934
- ISSN
- 1559-1182
- DOI
- 10.1007/s12035-012-8267-8
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neuronal Survival (013212041)
- id
- 19715463-8014-4c4d-a74a-c32fd43fc41b (old id 2609345)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/22544647?dopt=Abstract
- date added to LUP
- 2016-04-01 10:27:58
- date last changed
- 2022-05-17 23:15:15
@article{19715463-8014-4c4d-a74a-c32fd43fc41b,
abstract = {{Parkinson's disease patients exhibit progressive spreading of aggregated α-synuclein in the nervous system. This slow process follows a specific pattern in an inflamed tissue environment. Recent research suggests that prion-like mechanisms contribute to the propagation of α-synuclein pathology. Little is known about factors that might affect the prion-like behavior of misfolded α-synuclein. In this review, we suggest that neuroinflammation plays an important role. We discuss causes of inflammation in the olfactory bulb and gastrointestinal tract and how this may promote the initial misfolding and aggregation of α-synuclein, which might set in motion events that lead to Parkinson's disease neuropathology. We propose that neuroinflammation promotes the prion-like behavior of α-synuclein and that novel anti-inflammatory therapies targeting this mechanism could slow disease progression.}},
author = {{Lema Tomé, Carla and Tyson, Trevor and Rey, Nolwen and Grathwohl, Stefan and Britschgi, Markus and Brundin, Patrik}},
issn = {{1559-1182}},
language = {{eng}},
number = {{2}},
pages = {{561--574}},
publisher = {{Humana Press}},
series = {{Molecular Neurobiology}},
title = {{Inflammation and α-Synuclein's Prion-like Behavior in Parkinson's Disease-Is There a Link?}},
url = {{http://dx.doi.org/10.1007/s12035-012-8267-8}},
doi = {{10.1007/s12035-012-8267-8}},
volume = {{47}},
year = {{2013}},
}