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

被引：14

作者：

Chan, Daniel Kam Yin ^{[1
,2
,3
]}

Xu, Ying Hua ^{[1
,2
,3
]}

Chan, Luke Kar Man ^{[4
]}

Braidy, Nady ^{[1
,2
,3
]}

Mellick, George D. ^{[5
]}

机构：

[1] Bankstown Hosp, Dept Aged Care & Rehabil, Bankstown, NSW 2200, Australia

[2] Ingham Inst, Liverpool, NSW 2170, Australia

[3] Univ New South Wales, Fac Med, Sydney, NSW, Australia

[4] Griffith Univ, Fac Med Sci, Nathan, Qld, Australia

[5] Griffith Univ, Griffith Inst Drug Discovery, Nathan, Qld, Australia

来源：

TRANSLATIONAL NEURODEGENERATION | 2017年 / 6卷

关键词：

Parkinson's disease; alpha-synuclein; Endocytosis; Aggregation; LEWY BODY; PATHOLOGY; NEURODEGENERATION; TRANSMISSION; SYSTEM; MODEL;

D O I：

10.1186/s40035-017-0104-6

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

In this mini-review, we summarize recent findings relating to the prion-like propagation of a-synuclein (alpha-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 alpha-syn (via exocytosis and endocytosis). The classical accumulation of aggregated a-syn in PD may result from an increased production or a failure in the mechanisms of clearance of alpha-syn. We discuss novel agents, currently in clinical trial for PD including the ones that impact the aggregation of alpha-syn and others that interfere with a-syn endocytosis as a means to target the progression of the disease.

引用

页数：5

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