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Archived Comments for: Docosahexaenoic and eicosapentaenoic acids increase prion formation in neuronal cells

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  1. Offence or defence?

    Andrew Carmichael, University of Central Lancashire

    29 September 2008

    In view of the work of Ruth Itzhaki at Manchester on HSV1 in AD showing 'entombment' of virus in amyloid deposits (mis-folded proteins) and the interpretation of this as a defensive mechanism it seems possible that the effects shown in this article are a parallel of the same style of CNS defence. The use of the prion to form its own 'tomb' is a smart move and the resultant product should not be viewed as the cause of the disease. This assumption of 'cause' rather than defence has resulted in years of blind alley research in AD and should be taken into account here. Amyloid is 'landfill' or garbage disposal and not the cause of AD. Similarly the disrupted protein metabolism with resources diverted to defence in the neuron is the cause of CJD and not the prion per se.

    Competing interests

    No competing interests