Dissecting the potential molecular mechanisms underlying alpha-synuclein cell-to-cell transfer in Parkinson's disease.
(2009) In Parkinsonism & Related Disorders 15 Suppl 3. p.143-147- Abstract
- Alpha-synuclein (alpha-syn) aggregation is central to neuropathological changes in Parkinson's disease. The aggregates spread within the central nervous system according to a very predictable pattern. A prion-like transmission of alpha-syn aggregates has been recently proposed to explain this propagation pattern. First, we review the growing evidence for such a mechanism. This process is likely to occur in three consecutive steps: (i) exit of alpha-syn template from the donor cell, (ii) entry to the recipient cell and (iii) initiation of the nucleation. In a second part, we discuss the possible underlying mechanisms for each of these steps, based on our current knowledge about how cells handle alpha-syn but also other proteins involved in... (More)
- Alpha-synuclein (alpha-syn) aggregation is central to neuropathological changes in Parkinson's disease. The aggregates spread within the central nervous system according to a very predictable pattern. A prion-like transmission of alpha-syn aggregates has been recently proposed to explain this propagation pattern. First, we review the growing evidence for such a mechanism. This process is likely to occur in three consecutive steps: (i) exit of alpha-syn template from the donor cell, (ii) entry to the recipient cell and (iii) initiation of the nucleation. In a second part, we discuss the possible underlying mechanisms for each of these steps, based on our current knowledge about how cells handle alpha-syn but also other proteins involved in neurodegenerative diseases with a prion-like propagation. Finally, we discuss which molecular species of alpha-syn (monomer, oligomer, fibril) could be the seeding-competent species and whether this seeding process could be a common mechanism in neurodegenerative diseases. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1540493
- author
- Angot, Elodie LU and Brundin, Patrik LU
- organization
- publishing date
- 2009
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Parkinsonism & Related Disorders
- volume
- 15 Suppl 3
- pages
- 143 - 147
- publisher
- Elsevier
- external identifiers
-
- pmid:20082977
- scopus:71849117852
- ISSN
- 1873-5126
- DOI
- 10.1016/S1353-8020(09)70802-8
- 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
- 42897ebe-57fc-49c4-985f-b8a665904e6a (old id 1540493)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/20082977?dopt=Abstract
- date added to LUP
- 2016-04-04 07:07:38
- date last changed
- 2022-03-23 00:43:35
@article{42897ebe-57fc-49c4-985f-b8a665904e6a, abstract = {{Alpha-synuclein (alpha-syn) aggregation is central to neuropathological changes in Parkinson's disease. The aggregates spread within the central nervous system according to a very predictable pattern. A prion-like transmission of alpha-syn aggregates has been recently proposed to explain this propagation pattern. First, we review the growing evidence for such a mechanism. This process is likely to occur in three consecutive steps: (i) exit of alpha-syn template from the donor cell, (ii) entry to the recipient cell and (iii) initiation of the nucleation. In a second part, we discuss the possible underlying mechanisms for each of these steps, based on our current knowledge about how cells handle alpha-syn but also other proteins involved in neurodegenerative diseases with a prion-like propagation. Finally, we discuss which molecular species of alpha-syn (monomer, oligomer, fibril) could be the seeding-competent species and whether this seeding process could be a common mechanism in neurodegenerative diseases.}}, author = {{Angot, Elodie and Brundin, Patrik}}, issn = {{1873-5126}}, language = {{eng}}, pages = {{143--147}}, publisher = {{Elsevier}}, series = {{Parkinsonism & Related Disorders}}, title = {{Dissecting the potential molecular mechanisms underlying alpha-synuclein cell-to-cell transfer in Parkinson's disease.}}, url = {{http://dx.doi.org/10.1016/S1353-8020(09)70802-8}}, doi = {{10.1016/S1353-8020(09)70802-8}}, volume = {{15 Suppl 3}}, year = {{2009}}, }