Acta Neuropathologica

, 112:1 | Cite as

Koch’s postulates and infectious proteins

  • Lary Walker
  • Harry LeVine
  • Mathias Jucker
Hypothesis Paper


Koch’s postulates were formulated in the late nineteenth century as guidelines for establishing that microbes cause specific diseases. Because the rules were developed for living agents—particularly bacteria—their applicability to inanimate pathogens such as viruses and infectious proteins has been problematic. The unorthodox mechanism by which prion diseases are transmitted, involving specific physicochemical characteristics of the protein as well as susceptibility traits of the host, has made these disorders refractory to analysis within the context of the original Koch’s postulates. In addition, evidence is accumulating that other proteopathies, such as AA amyloidosis, apolipoprotein AII amyloidosis, and cerebral Aβ amyloidosis, can be induced in vulnerable recipients by cognate proteinaceous agents. In light of the salient differences in the mode of disease-transmission by microbes and proteins, we propose modifications of Koch’s postulates that will specifically accommodate presumed infectious proteins.


Alzheimer’s disease Amyloid Apolipoprotein AII Conformational disease Prion 



We thank Ingo Autenrieth, John Hardy, Jens Pahnke, Rebecca Rosen, Margaret Walker and Rolf Warzok for helpful discussions. This work was supported by grants from the Woodruff Foundation, NIH (RR-00165), by the Sanders-Brown Center on Aging and Chandler Medical Center of the University of Kentucky, and by the Alzheimer’s Association.


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Copyright information

© Springer-Verlag 2006

Authors and Affiliations

  1. 1.Yerkes National Primate Research Center and Department of Neurology Emory UniversityAtlantaUSA
  2. 2.Center on Aging, Department of Molecular and Cellular Biochemistry University of KentuckyLexingtonUSA
  3. 3.Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research University of TübingenTübingenGermany

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