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  • A cross-study transcriptional analysis of Parkinson's disease

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    Author(s)
    Sutherland, Greg T
    Matigian, Nicholas A
    Chalk, Alistair M
    Anderson, Matthew J
    Silburn, Peter A
    Mackay-Sim, Alan
    Wells, Christine A
    Mellick, George D
    Griffith University Author(s)
    Mackay-Sim, Alan
    Silburn, Peter A.
    Matigian, Nicholas
    Anderson, Matthew J.
    Mellick, George
    Wells, Christine
    Sutherland, Greg T.
    Chalk, Alistair M.
    Year published
    2009
    Metadata
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    Abstract
    The study of Parkinson's disease (PD), like other complex neurodegenerative disorders, is limited by access to brain tissue from patients with a confirmed diagnosis. Alternatively the study of peripheral tissues may offer some insight into the molecular basis of disease susceptibility and progression, but this approach still relies on brain tissue to benchmark relevant molecular changes against. Several studies have reported whole-genome expression profiling in post-mortem brain but reported concordance between these analyses is lacking. Here we apply a standardised pathway analysis to seven independent case-control studies, ...
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    The study of Parkinson's disease (PD), like other complex neurodegenerative disorders, is limited by access to brain tissue from patients with a confirmed diagnosis. Alternatively the study of peripheral tissues may offer some insight into the molecular basis of disease susceptibility and progression, but this approach still relies on brain tissue to benchmark relevant molecular changes against. Several studies have reported whole-genome expression profiling in post-mortem brain but reported concordance between these analyses is lacking. Here we apply a standardised pathway analysis to seven independent case-control studies, and demonstrate increased concordance between data sets. Moreover data convergence increased when the analysis was limited to the five substantia nigra (SN) data sets; this highlighted the down regulation of dopamine receptor signaling and insulin-like growth factor 1 (IGF1) signaling pathways. We also show that case-control comparisons of affected post mortem brain tissue are more likely to reflect terminal cytoarchitectural differences rather than primary pathogenic mechanisms. The implementation of a correction factor for dopaminergic neuronal loss predictably resulted in the loss of significance of the dopamine signaling pathway while axon guidance pathways increased in significance. Interestingly the IGF1 signaling pathway was also over-represented when data from non-SN areas, unaffected or only terminally affected in PD, were considered. Our findings suggest that there is greater concordance in PD whole-genome expression profiling when standardised pathway membership rather than ranked gene list is used for comparison.
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    Journal Title
    PloS One
    Volume
    4
    Issue
    3
    Publisher URI
    http://www.plosone.org/home.action
    DOI
    https://doi.org/10.1371/journal.pone.0004955
    Copyright Statement
    © 2009 Sutherland et al. This is an Open Access article distributed under the terms of the Creative Commons Attribution License CCAL. (http://www.plos.org/journals/license.html)
    Subject
    Neurology and neuromuscular diseases
    Publication URI
    http://hdl.handle.net/10072/25755
    Collection
    • Journal articles

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