Increased propensity for amyloidogenesis in male mice

Shmuel Shtrasburg*, Mordechai Pras, Mordechai Dulitzky, Clara Pariente, Rivka Gal, Adam Mor, Avi Livneh

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Background. The male sex is a risk factor for reactive amyloidogenesis in several disease entities. Environmental, socioeconomic or genetic factors may underlie this male preponderance. This study was aimed at discovering whether male sex predisposes to reactive amyloidosis also in mice and to elucidate some of the hormonal associations of this risk. Methods. Male and female Swiss mice were subjected to an established amyloid induction protocol and the amount of their splenic amyloid was determined and compared. The effect of estrogen, progesterone, testosterone and adrenalin on amyloidogenesis was studied in both sexes by administering these hormones during amyloid induction and comparing the amount of splenic amyloid of the study mice with the control mice which received the amyloid induction protocol alone. Results. Amyloid deposition appeared to be more abundant in male mice. This gender difference was not associated with any of the 3 sex hormones tested. Despite an expected increment, adrenalin caused an attenuation of amyloid deposition. Conclusions. The preferential expression of reactive amyloidosis in male mice seems to be unrelated to the common sex hormones. Increased production of other hormones such as adrenalin, or perhaps an augmented susceptibility to their effect, may cause gender differences by suppressing female amyloidogenesis. Our study favors the hypothesis of genetic predisposition as the mechanism leading to sex differences in amyloidogenesis. Further validation of our findings in gonadal ablated models and other amyloid induction protocols is warranted.

Original languageEnglish
Pages (from-to)421-426
Number of pages6
JournalClinical and Experimental Rheumatology
Issue number4
StatePublished - Jul 2004


  • Adrenalin
  • Amyloid A
  • Amyloid enhancing factor
  • Animal model
  • Sex hormones


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