Loss of Hair Pigment Linked to Nervous System Disorders

The findings were published in the January 31, 2003, issue of Science.

Investigators from Cornell University (Ithaca, NY, USA) and Stanford University (Stanford, CA, USA) genetically engineered a line of mice lacking the mahoganoid gene. These mice were similar in phenotype to mice lacking the Attractin (Atrn) gene. Attractin is a highly conserved integral membrane protein that functions in the maintenance of neural system architecture, immune cell interactions, and neuropeptide presentation regulating pigmentation.

The mahoganoid mice had brain malformations similar to those seen in cows with BSE. However, senior author Dr. Teresa M. Gunn, assistant professor of genetics in Cornell's College of Veterinary Medicine explained, "We do see the same kind of tissue degeneration -- with fluid-filled vacuoles, or holes, where the gray matter should be -- in BSE cattle with bovine spongiform encephalopathy and in these mutant mice. But the mice do not have the same motor coordination problems as mad cows, and the condition is not lethal.”

The authors concede that mahoganoid mice do not provide a model for the study of BSE, since prion particles are not involved. On the other hand, the mice could be valuable animal models for human disorders, such as Parkinson's and Alzheimer's disease.