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Editorial commentary
Could immunological mechanisms trigger neurodegeneration in frontotemporal dementia?
  1. James R Burrell1,2,
  2. John R Hodges1,2
  1. 1Neuroscience Research Australia, Sydney, New South Wales, Australia
  2. 2University of New South Wales, Sydney, New South Wales, Australia
  1. Correspondence to Professor John R Hodges, Neuroscience Research Australia, Cnr Barker St and Easy St, Randwick, Sydney, NSW 2031, Australia; j.hodges{at}neura.edu.au

http://dx.doi.org/10.1136/jnnp-2013-304936

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    Non-thyroid autoimmune disease is more common in frontotemporal dementia caused by Tar-DNA binding protein-43 (TDP-43).

    When conveying a new diagnosis of frontotemporal dementia (FTD) the clinician almost invariably encounters the following questions ‘Why has this happened?’ ‘Is there any treatment?’ and ‘Will our children get it?’ With the discovery of the MAPT and Progranulin mutations, and most recently pathological C9ORF72 repeat expansions,1 we have a much firmer handle on the last question. These discoveries have undoubtedly shed light on the pathogenesis and final common pathway in FTD but we still know little about causation in sporadic cases. Without a clear understanding …

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    Footnotes

    • Contributors JRB and JRH drafted and revised the submission. Both authors have approved the final version.

    • Competing interests None.

    • Provenance and peer review Commissioned; internally peer reviewed.

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