Mini-review on initiatives to interfere with the propagation and clearance of alpha-synuclein in Parkinson's disease

Daniel Kam Yin Chan; Ying Hua Xu; Luke Kar Man Chan; Nady Braidy; George D. Mellick

doi:10.1186/s40035-017-0104-6

Mini-review on initiatives to interfere with the propagation and clearance of alpha-synuclein in Parkinson's disease

Daniel Kam Yin Chan, Ying Hua Xu, Luke Kar Man Chan, Nady Braidy, George D. Mellick

Western Sydney University

Research output: Contribution to journal › Article › peer-review

Abstract

In this mini-review, we summarize recent findings relating to the prion-like propagation of α-synuclein (α-syn) and the development of novel therapeutic strategies to target synucleinopathy in Parkinson's disease (PD). We link the Braak's staging hypothesis of PD with the recent evidence from in-vivo and in-vitro studies for the prion-like cell-to-cell propagation of α-syn (via exocytosis and endocytosis). The classical accumulation of aggregated α-syn in PD may result from an increased production or a failure in the mechanisms of clearance of α-syn. We discuss novel agents, currently in clinical trial for PD including the ones that impact the aggregation of α-syn and others that interfere with α-syn endocytosis as a means to target the progression of the disease.

Original language	English
Article number	33
Number of pages	5
Journal	Translational Neurodegeneration
Volume	6
Issue number	1
DOIs	https://doi.org/10.1186/s40035-017-0104-6
Publication status	Published - 2017

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© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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abstract = "In this mini-review, we summarize recent findings relating to the prion-like propagation of α-synuclein (α-syn) and the development of novel therapeutic strategies to target synucleinopathy in Parkinson's disease (PD). We link the Braak's staging hypothesis of PD with the recent evidence from in-vivo and in-vitro studies for the prion-like cell-to-cell propagation of α-syn (via exocytosis and endocytosis). The classical accumulation of aggregated α-syn in PD may result from an increased production or a failure in the mechanisms of clearance of α-syn. We discuss novel agents, currently in clinical trial for PD including the ones that impact the aggregation of α-syn and others that interfere with α-syn endocytosis as a means to target the progression of the disease.",

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AU - Chan, Daniel Kam Yin

AU - Xu, Ying Hua

AU - Chan, Luke Kar Man

AU - Braidy, Nady

AU - Mellick, George D.

PY - 2017

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AB - In this mini-review, we summarize recent findings relating to the prion-like propagation of α-synuclein (α-syn) and the development of novel therapeutic strategies to target synucleinopathy in Parkinson's disease (PD). We link the Braak's staging hypothesis of PD with the recent evidence from in-vivo and in-vitro studies for the prion-like cell-to-cell propagation of α-syn (via exocytosis and endocytosis). The classical accumulation of aggregated α-syn in PD may result from an increased production or a failure in the mechanisms of clearance of α-syn. We discuss novel agents, currently in clinical trial for PD including the ones that impact the aggregation of α-syn and others that interfere with α-syn endocytosis as a means to target the progression of the disease.

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DO - 10.1186/s40035-017-0104-6

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JO - Translational Neurodegeneration

JF - Translational Neurodegeneration

IS - 1

M1 - 33

ER -

Mini-review on initiatives to interfere with the propagation and clearance of alpha-synuclein in Parkinson's disease

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