Amyloid resistance in A/J mice is determined by a single gene


WIDESPREAD tissue deposition of the unique fibrous protein amyloid occurs in a variety of human diseases1. ‘Secondary’ amyloidosis arises as a complication of chronic infectious or inflammatory disease and an identical syndrome can be induced in mice by repeated injections of casein2. Little genetic work has been done in this area, probably because development of amyloidosis is often variable, even with a standard induction regimen, and results are inconsistent3. Furthermore, because of the many complex immunological aberrations occurring during the amyloid induction period4, the various experimental manipulaions which can affect it4, and the wide range of induction times seen in different murine strains2, on would expect that multiple genes and alleles would influence amyloidogenesis. Nevertheless, the discovery of the uniquely resistant A strain5 suggested the posiblity of isolating at least part of the genetic analysis of amyloid induction in two inbred strains, CBA/J and A/J, differing markedly in susceptibility to amyloidosis5. We show for the first time that a single gene confers resistance on the A/J strain. Our results imply that genetic factors may also define subpopulations of chronic disease patients who are at greater risk from amyloid disease.

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WOHLGETHAN, J., CATHCART, E. Amyloid resistance in A/J mice is determined by a single gene. Nature 278, 453–454 (1979).

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