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Accumulation of dysfunctional SOD1 protein in Parkinson’s disease is not associated with mutations in the SOD1 gene

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Acknowledgements

Tissues were received from the New South Wales Tissue Resource Centre at the University of Sydney, supported by the Schizophrenia Research Institute and the National Institute of Alcohol Abuse and Alcoholism (NIH (NIAAA) R24AA012725), from the Sydney Brain Bank, which is supported by Neuroscience Research Australia and the University of New South Wales.

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Authors and Affiliations

  1. Discipline of Biomedical Science and Brain and Mind Centre, Sydney Medical School, The University of Sydney, Sydney, NSW, 2006, Australia

    Benjamin G. Trist & Kay L. Double

  2. Faculty of Medicine and Health Sciences, Department of Biomedical Sciences, Macquarie University, Sydney, NSW, 2109, Australia

    Jennifer A. Fifita, Sarah E. Freckleton & Ian P. Blair

  3. The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, 3052, Australia

    Dominic J. Hare

  4. Elemental Bio-Imaging Facility, University of Technology Sydney, Broadway, NSW, 2007, Australia

    Dominic J. Hare

  5. Department of Pathology, The University of Melbourne, Parkville, VIC, 3052, Australia

    Dominic J. Hare

  6. Healthy Brain Ageing Program, University of Sydney, Sydney, NSW, 2006, Australia

    Simon J. G. Lewis

  7. Royal Prince Alfred Hospital, Camperdown, NSW, 2050, Australia

    Simon J. G. Lewis

  8. Central Clinical School and Brain and Mind Centre, Sydney Medical School, The University of Sydney, Sydney, NSW, 2006, Australia

    Glenda M. Halliday

Authors
  1. Benjamin G. Trist
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  2. Jennifer A. Fifita
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  3. Sarah E. Freckleton
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  4. Dominic J. Hare
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  5. Simon J. G. Lewis
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  6. Glenda M. Halliday
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  7. Ian P. Blair
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  8. Kay L. Double
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Contributions

B.G.T. and K.L.D. designed the study. B.G.T. and K.L.D. applied for all human tissues. B.G.T. and K.L.D. raised funds for the study. B.G.T. and K.L.D. gained human research ethics approval. S.J.G.L. and G.M.H. provided clinical information for all human tissue cases obtained. J.A.F, S.E.F and I.P.B performed the experiments and analyzed the data. B.G.T., D.J.H. and K.L.D. wrote drafts of the manuscript. All authors edited the manuscript.

Corresponding author

Correspondence to Kay L. Double.

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Conflict of interest

The authors declare no competing financial interests or conflicts of interest.

Funding

This work was supported by funds from Parkinson’s NSW (2015 and 2016 seed grants) and the University of Sydney (Biomedical Science, BRIG).

Data availability

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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Trist, B.G., Fifita, J.A., Freckleton, S.E. et al. Accumulation of dysfunctional SOD1 protein in Parkinson’s disease is not associated with mutations in the SOD1 gene. Acta Neuropathol 135, 155–156 (2018). https://doi.org/10.1007/s00401-017-1779-6

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  • DOI: https://doi.org/10.1007/s00401-017-1779-6

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