ISSN: 2161-0460

Journal of Alzheimers Disease & Parkinsonism
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  • Research Article   
  • J Alzheimers Dis Parkinsonism 2017, Vol 7(5): 370
  • DOI: 10.4172/2161-0460.1000370

Endothelial Degeneration of Parkinson's Disease is Related to Alpha-Synuclein Aggregation

Panzao Yang1,2,3, Xiao-Li Min1,2,3,4,5, Mojdeh Mohammadi1,2,3,6, Clinton Turner2,7, Richard Faull2,8, Henry Waldvogel2,8, Mike Dragunow1,2 and Jian Guan1,2*
1Faculty of Medical and Health Sciences, Department of Pharmacology and Clinical Pharmacology, University of Auckland, New Zealand
2Faculty of Medical and Health Sciences, University of Auckland, Centre for Brain Research, New Zealand
3Faculty of Medical and Health Sciences, Liggins Institute, University of Auckland, New Zealand
4Faculty of Clinical Medicine, Yunnan University of Traditional Chinese Medicine, China
5The First Affiliated Hospital, Yunnan University of Traditional Chinese Medicine, China
6Department of Toxicology and Pharmacology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran
7Department of Anatomical Pathology, , LabPlus, Auckland City Hospital Auckland, New Zealand
8Faculty of Medical and Health Sciences, Department of Anatomy and Medical Imaging, University of Auckland, New Zealand
*Corresponding Author : Jian Guan, Faculty of Medical and Health Sciences, Department of Pharmacology and Clinical Pharmacology, University of Auckland, Private Bag 92019 Auckland 1023, New Zealand, Tel: 0064-9-9236134, Email: j.guan@auckland.ac.nz

Received Date: Aug 20, 2017 / Accepted Date: Aug 29, 2017 / Published Date: Sep 06, 2017

Abstract

Objective: We previously reported that the ability of vascular remodelling is impaired in human Parkinson’s disease, leading to endothelial degeneration and vascular dysfunction. Aggregation of α-synuclein is a hallmark of neurodegeneration in Parkinson’s disease and inflammation and autophagy may contribute to secondary neuronal degeneration. The current study examined the association between these characteristic pathologies and endothelial cell degeneration in Parkinson’s disease.
Methods: The study used the post-mortem grey matter from middle frontal gyrus (MFG) of human Parkinson’s disease and age-matched control cases. Immunohistochemical staining of phosphorylated α-synuclein, p62 for autophagy, Human Leukocyte Antigen-antigen D Related (HLA-DR) for activated microglia, Factor VIII for endothelial cells and Neuronal Nuclei for neurons were performed using either tissue microarray or free-floating sections. The expression of these factors were quantified by analysing the images of the stained sections and compared between the Parkinson’s disease and the age-matched control groups.
Results: Compared to the control cases the expression of phosphorylated α-synuclein and p62 was increased in Parkinson’s disease, whereas both neurons and endothelial cells were significantly reduced, with no changes in the number of microglial cells. The density of phosphorylated α-synuclein was negatively correlated with the total length of endothelial cell associated blood vessels when compared across normal and Parkinson’s disease cases combined. However, using double label immunohistochemistry we found that the degree of endothelial cell degeneration in Parkinson’s disease was not directly related to the degree of neuronal degeneration and accumulation of phosphorylated α-synuclein.
Conclusion: α-synuclein and autophagy are associated with endothelial degeneration in Parkinson’s disease. The degree of endothelial degeneration was not related to the extent of neuronal degeneration, both of which were copathological changes in PD brains. Alpha-synuclein-associated endothelial degeneration was also age-related pathology.

Keywords: Alpha-synuclein; Endothelial degeneration; Autophagy; Parkinson’s diseases; Human; Immunohistochemistry

Citation: Yang P, Min XL, Mohammadi M, Turner C, Faull R, et al. (2017) Endothelial Degeneration of Parkinson’s Disease is Related to Alpha-Synuclein Aggregation. J Alzheimers Dis Parkinsonism 7: 370. Doi: 10.4172/2161-0460.1000370

Copyright: © 2017 Yang P, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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