. Amyloid-β pathology and cerebral amyloid angiopathy are frequent in iatrogenic Creutzfeldt-Jakob disease after dural grafting. Swiss Med Wkly. 2016;146:w14287. Epub 2016 Jan 26 PubMed.


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  1. The recent reports from the Aguzzi/Budka and Collinge/Brandner laboratories reminded me that we were possibly the first to describe Aβ deposition in iatrogenic CJD, in 1989 and 1996 in a 56-year-old man (Simpson et al., 1996). We thought that the concurrence of CJD and AD-like lesions was "an unusual feature," especially in the absence of neurofibrillary tangles. These observations were published in rather obscure Australian journals, and have been lost in the plethora of subsequent papers on this this subject.

    In the ensuing years, many have noted the occasional case of CJD in which neurofibrillary/neuritic changes occur, and the frequent occurrence in which aggressive forms of Aβ deposition in autosomal-dominant AD are associated with α-synuclein aggregates, and indeed most cases of dementia with Lewy bodies are associated with Aβ deposition.

    The co-deposition of two distinct forms of amyloidogenic proteins is common, indeed it is the hallmark of AD in which Aβ drives tau aggregation. The whole story reminds me of the principle underlying the "amyloid-enhancing factor," first described in the early 1960s, in which systemic serum amyloid A (SAA) protein was found to drive its own propensity to aggregate.

    No doubt, one day all these self-seeding and cross-seeding interactions will be clearly understood in mechanistic terms. In the meantime, it's great that neuropathologists should delve into their archives and use the latest technologies to uncover the lesions we have missed over the years.


    . Iatrogenic Creutzfeldt-Jakob disease and its neurosurgical implications. J Clin Neurosci. 1996 Apr;3(2):118-23. PubMed.

    View all comments by Colin Masters
  2. I think this paper is interesting for several reasons, not least of which is the fact that it appears to reproduce an earlier finding of increased amyloid in a recipient of a dura transplant. Also, it is telling that again there is no detectable tau pathology. This implies that there is no transmission of tau or that transmission takes a very long time to manifest. With respect to Aβ, it is interesting and consistent with Jaunmuktane et al., 2015, in that dura transplants have parenchymal amyloid and less CAA, whereas peripherally administered hGH cases had mostly CAA.

    View all comments by Dominic Walsh

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