economic impact of HD on the public at large tends to be relatively minimal. However, on a lesser scale, Huntington's disease can have devastating consequences for specific afflicted families.
The assorted neurologic and psychiatric symptoms of HD are associated with the premature loss of neurons in the brain. Typically, these symptoms include involuntary choreiform movements and dementia (Gusella, 1991, p. 125).
Certain features of Huntington's disease have caused it to be the subject of much investigation. For one, HD appears to result from a fully dominant, autosomal mutation (Laird, 1990, p. 242). This means that there is no difference between the symptoms of homozygous mutant individuals (i.e., those that have two defective genes) and those of heterozygotes (i.e., people with one defective and one normal gene).
A second interesting characteristic of HD is the variability of its age of onset (Laird, 1990, p. 242). For instance, there is a very early onset form. This form may actually occur before the age of 10 years. In addition, there is a late onset form; this type of HD is typically first found in the elderly (Clarke & Bundey, 1990, p. 180).
Finally, the last intriguing aspect of Huntington's disease relates to the source of a victim's genetic defect and its association with age of onset (Laird, 1990, p. 242). For example, it seems that the juvenile onset form of HD occurs more frequently in individuals who have inherited their defective gene from their fathers (Laird, 1990, p. 242). Some have even surmised that the early onset phenotypes result from a sort of gene "imprinting" (Laird, 1990, p. 242). Such imprinting which would occur in the victim's fathers might involve some kind of developmental process. Ultimately, this processing could affect the gene's subsequent functioning (Laird, 1990, p. 242).
All of the interest in Huntington's disease has resulted in an increased understanding of the ...