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E-GEOD-54282 - System-based analyses of brain regions functionally impacted in Parkinson's disease reveals underlying causal mechanisms
Released on 1 September 2014, last updated on 22 August 2016
Detailed analysis of disease-affected tissue provides insight into molecular mechanisms contributing to pathogenesis. Substantia nigra, striatum and cortex are functionally connected with increasing degrees of alpha-synuclein pathology in Parkinson's disease. Functional and causal pathway analysis of gene expression and proteomic alterations in these three regions revealed pathways that correlated with deposition of alpha-synuclein. Microarray and RNAseq experiments revealed previously unidentified causal changes related to oligodendrocyte function and synaptic vesicle release and other changes were reflected across all brain regions. Importantly a subset of these changes were replicated in Parkinson's disease blood. Proteomic assessment revealed alterations in mitochondria and vesicular transport proteins that preceded gene gene expression changes indicating defects in translation and/or protein turnover. Our combined approach of proteomics, RNAseq and microarray analyses provides a comprehensive view of the molecular changes that accompany alpha-synculein pathology in Parkinson's disease, and may be instrumental in understanding and diagnosing Parkinson's disease progression. Substantia Nigra (3 normal, 3 PD), Striatum (6 normal, 6 PD), Cortex (5 normal, 5 PD), Cortex non-PD neurodegeneration (2 normal, 3 DLB). Note Sample X201264 was used both for Cortex normal and for Cortex nonPD normal
transcription profiling by array
Brigit Erin Riley <email@example.com>, Alexander E Ivliev, Birgit Schule, Brigit E Riley, Dorothea Emig-Agius, Glenda M Halliday, J W Langston, Jeff Alexander, Jennifer A Johnston, Marina Bessarabova, Scott Braxton, Shyra J Gardai, Ted Yednock, Thomas Shaler, William Wallace
Systems-based analyses of brain regions functionally impacted in Parkinsons disease reveals underlying causal mechanisms. Riley BE, Gardai SJ, Emig-Agius D, Bessarabova M, Ivliev AE, Schüle B, Schüle B, Alexander J, Wallace W, Halliday GM, Langston JW, Braxton S, Yednock T, Shaler T, Johnston JA. :e102909 (2014), PMID:25170892