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Hindi Research Article
Preliminary Set Theory-Type Analysis of Proteins Associated With Parkinson's Disease
Paul Whitesman*
Disease Motifs, Rochdale, Greater Manchester, England
- Corresponding Author:
- Paul Whitesman
Disease Motifs, Rochdale, Greater Manchester, England
Tel: ++44 (0) 1706 343120
E-mail: paulwhitesman@diseasemotifs.co.uk
Received date: September 29, 2014; Accepted date: November 11, 2014; Published date: November 18, 2014
Citation: Whitesman P (2014) Preliminary Set Theory-Type Analysis of Proteins Associated With Parkinson’s Disease. J Alzheimers Dis Parkinsonism 4:170. doi: 10.4172/2161-0460.1000170
Copyright: © 2014 Whitesman P. 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.
Abstract
In an attempt to create a model of Parkinson’s disease (PD) eighty-three proteins were extracted from the Swiss- Prot protein database that had some casual mention of PD. These were split up into various subsets of proteins of which three are focused on here: PARK, made up of proteins that had some indication that polymorphisms in the protein might increase a person’s susceptibility to develop PD; MITOCHOND, proteins which had some association with the mitochondria; and MT-C1D, proteins that were implicated in mitochondrial complex 1 deficiency. The PARK subset had 21 out of 83 proteins (21/83); MITOCHOND 33 out of 83 proteins (33/83); and MT-C1D 17 out of 83 proteins (17/83). The results could be used to build up a basic model of PD creating phenotypes based on sets of proteins. The main phenotypes established here are; non-mitochondrial PD (50/83) and mitochondrial PD (33/83). Further division is possible dependant on whether proteins have polymorphisms which increase susceptibility to develop PD. MT-C1D seems to be independent of the PARK set. This is a very simplistic attempt at trying to model Parkinson’s disease at the proteomic level and will need further work to build up the more complex and realistic PD proteomic disease model.
