I’m having a problem with your thesis. PD in general occurs at a higher frequency than you suggest. There are dominant and recessive genes involved.

That said, begin with this link and scroll down to Parkinson’s. There is a predisposition to PD due to differences in the nucleotides. This is from and article published 11/2008
http://www.sciencedaily.com/releases/2008/11/081124102659.htm

Parkinson’s is associated with a few genes, some dominant and some recessive.

Because there are also environmental and exposure triggers and possible receptor blockers such as smoking, genes alone do not seem to be the complete story
http://www.medterms.com/script/main/art.asp?articlekey=25045

Genetics seems to play more of a role in young onset PD rather than the more common Parkinson’s disease affecting people around 50-60 years and up.

The press release from 2003 published in The National Institute of Neurological Disorders and Strokes
http://www.ninds.nih.gov/news_and_events/press_releases/pressrelease_parkinson_synuclein_103003.htm
points to a direction of research, it is not an answer in itself.

Where did you find the 1:10000 ratio? It appears to be closer to 2:10000?
http://www.pscky.org/Dot_Faqs.asp?faqid=18

Believe me, when you are in otherwise good health and still have most of your body strength, it is difficult to read "old age" for 50-65 years of age. We tend to think that because those are the years around retirement age or used to be; PD makes going into older age very difficult and unpleasant.

No doctorate here, just saw your question and I’m gonna guess it’s because that particular dominant gene is rare in our population. It may be dominant, but it may still be very rare in today’s society.

you answered it yourself. There is a low gene frequency in the human gene pool for this particular disease.

Until very recently, researchers focused on possible environmental factors as the culprit in Parkinson’s disease. However, in 1996, mutations in the alpha-synuclein gene were identified in a few large families in whom the disease was unusually common. Since then, mutations in several other genes have also been linked to familial forms of Parkinson’s disease.

In this new study, investigators analyzed blood samples from another affected family, the "Iowa kindred," in which many relatives developed Parkinson’s disease or related neurological diseases. The family, followed by this team of researchers for many years, presented a puzzle to scientists because the genetic analyses of some family members initially showed no alpha-synuclein mutation. The scientists thought perhaps an entirely different genetic mutation might account for Parkinson’s disease in this family and had even given this other gene a name, PARK 4.

Not satisfied that they had the answer, scientists on the team decided to look again at genetic samples from the family, conducting additional analyses of the entire genome, including chromosome 4, the chromosome on which the alpha-synuclein gene is located.

****here’s a possible answer to your question: —-> In individuals in this family affected by Parkinson’s disease, instead of the usual *two* copies of the alpha-synuclein gene in the chromosome 4 pair, the researchers found *four* copies of the alpha-synuclein gene. This multiplication of the alpha-synuclein gene (an abnormal triplication of three genes on one chromosome 4 and the normal one copy on the other chromosome 4) results in the individual’s having too much synuclein. This protein buildup is believed to cause the Parkinson’s disease symptoms.