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Originally published online as doi:10.2353/ajpath.2007.070262 on June 14, 2007

Published online before print June 14, 2007
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(American Journal of Pathology. 2007;171:599-607.)
© 2007 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2007.070262

Doppel Induces Degeneration of Cerebellar Purkinje Cells Independently of Bax

Jiaxin Dong*, Aimin Li*, Naohiro Yamaguchi{dagger}, Suehiro Sakaguchi{ddagger} and David A. Harris*

From the Department of Cell Biology and Physiology,* Washington University School of Medicine, St. Louis, Missouri; the Department of Molecular Microbiology and Immunology,{dagger} Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan; and the Division of Molecular Cytology,{ddagger} Institute for Enzyme Research, University of Tokushima, Tokushima, Japan

Doppel (Dpl) is a prion protein paralog that causes neurodegeneration when expressed ectopically in the brain. To investigate the cellular mechanism underlying this effect, we analyzed Dpl-expressing transgenic mice in which the gene for the proapoptotic protein Bax had been deleted. We found that Bax deletion does not alter either clinical symptoms or Purkinje cell degeneration in Dpl transgenic mice. In addition, we observed that degenerating Purkinje cells in these animals do not display DNA fragmentation or caspase-3 activation. Our results suggest that non-Bax-dependent pathways mediate the toxic effects of Dpl in Purkinje cells, highlighting a possible role for nonapoptotic mechanisms in the death of these neurons.




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