Quick Search:

uzh logo
Browse by:
bullet
bullet
bullet
bullet

Zurich Open Repository and Archive

Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-61670

Durrenberger, Pascal F.; Grünblatt, Edna; Fernando, Francesca S.; Monoranu, Camelia Maria; Evans, Jordan; Riederer, Peter; Reynolds, Richard; Dexter, David T. (2012). Inflammatory pathways in Parkinson’s Disease; A BNE microarray study. Parkinson's Disease, 2012:ID 214714.

[img]
Preview
Published Version
PDF
984kB

View at publisher

Abstract

The aetiology of Parkinson's disease (PD) is yet to be fully understood but it is becoming more and more evident that neuronal cell death may be multifactorial in essence. The main focus of PD research is to better understand substantia nigra homeostasis disruption, particularly in relation to the wide-spread deposition of the aberrant protein α-synuclein. Microarray technology contributed towards PD research with several studies to date and one gene, ALDH1A1 (Aldehyde dehydrogenase 1 family, member A1), consistently reappeared across studies including the present study, highlighting dopamine (DA) metabolism dysfunction resulting in oxidative stress and most probably leading to neuronal cell death. Neuronal cell death leads to increased inflammation through the activation of astrocytes and microglia. Using our dataset, we aimed to isolate some of these pathways so to offer potential novel neuroprotective therapeutic avenues. To that effect our study has focused on the upregulation of P2X7 (purinergic receptor P2X, ligand-gated ion channel, 7) receptor pathway (microglial activation) and on the NOS3 (nitric oxide synthase 3) pathway (angiogenesis). In summary, although the exact initiator of striatal DA neuronal cell death remains to be determined, based on our analysis, this event does not remain without consequence. Extracellular ATP and reactive astrocytes appear to be responsible for the activation of microglia which in turn release proinflammatory cytokines contributing further to the parkinsonian condition. In addition to tackling oxidative stress pathways we also suggest to reduce microglial and endothelial activation to support neuronal outgrowth.

Citations

2 citations in Web of Science®
6 citations in Scopus®
Google Scholar™

Altmetrics

Downloads

34 downloads since deposited on 04 Apr 2012
18 downloads since 12 months

Detailed statistics

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Child and Adolescent Psychiatry
DDC:610 Medicine & health
Language:English
Date:2012
Deposited On:04 Apr 2012 08:28
Last Modified:30 Nov 2013 14:44
Publisher:Hindawi Publishing Corporation
ISSN:2090-8083
Additional Information:This article is only online. There is no print of the journal
Free access at:Official URL. An embargo period may apply.
Publisher DOI:10.1155/2012/214714
Official URL:http://www.hindawi.com/journals/pd/2012/214714

Users (please log in): suggest update or correction for this item

Repository Staff Only: item control page