iques above. This is so that the defective gene may be repaired before the onset of the disease. In order for this to be possible, the corrective gene must be isolated. Furthermore, the corrective gene must be good for transfer as well as a the proper vector to effectively execute the transfer. Because there is no cure for this illness, gene therapy may be the only answer if it is one day successful.ReferencesGuilleminault, C., Lugaresi, E., at el. Fatal Familial Insomnia: inherited prion diseases, sleep, and the thalamus. Raven Press, 1994. pp.15-20.Klug, W.S., Cummings, M.R. Concepts of Genetics. Prentice-Hall, Inc., 1994. pp. 425-427. Medori, R., Tritschler, H-J., at el. "Fatal Familial Insomnia, a Prion Disease with a Mutation at Codon 178 of the Prion Protein Gene" New England Journal of Medicine, 326 (7): 444-449 (1992). Petersen, R.B., Tabaton, M., at el. "Analysis of the prion Protein gene in Thalamic Dementia" Neurology, 42 (10): 1859-1863 (1992). Return Case Studies in Virtual Genetics 1996-1997Researchers discover new form of insomniaResearchers have discovered a brain-wasting disease that begins with severe insomnia and ends in hallucinations and death.The disease, sporadic fatal insomnia, is caused by the same type of deformed proteins, known as prions, that cause mad cow disease and its human variant, Creutzfeldt-Jakob disease, according to two studies.There is no known treatment or cure. It is not clear what causes the disease, but scientists know it is not inherited. And unlike one type of Creutzfeldt-Jakob disease, it is not believed to come from infected meat.Instead, scientists suspect it is caused by a spontaneous mutation in a single brain or nerve cell.So far, they have identified only six cases of the disease, but there could be others that were misdiagnosed as other mind-destroying illnesses such as Alzheimer's disease.Prions are proteins with Jekyll-and-Hyde personalities that cluster in the brain. When their mo...
