"There are at least 25 genes in the gene complex in which HOPA participates. Several of the genes are known to be involved with other forms of human illness. Because this polymorphism is relatively common and because we have human models of it, it can be used as a paradigm to understand those other gene defects," Philibert added.
The type of evolutionary advantage -- resistance to disease -- that the UI team saw in the HOPA polymorphism also can be seen in a polymorphism linked to sickle cell anemia. In that condition, one copy of the polymorphism causes mild cell abnormalities but also provides resistance to malaria and thus promotes human survival. However, two copies of the variant gene cause the debilitating disease sickle cell anemia.
In addition to Philibert's contributions, the UI study included work by Nancy C. Andreasen, M.D., Ph.D., the Andrew H. Woods Chair of Psychiatry at the UI. Raymond Crowe, M.D., the George Winokur Professor of Psychiatry at the UI, also provided assistance with the investigation.
Funding for the study included a grant from the Nellie Ball Trust for Schizophrenia Research, a grant from the National Alliance for Research on Schizophrenia and Depression and several grants from the National Institute of Mental Health (part of the NIH).
The abstract for the study is available online at www3.interscience.wiley/cgi-bin/abstract/107614465/ABSTRACT