BIO 100 Survey of Biosciences

Parkinson’s Disease Organismal/population level:
The objective of this paper is to relay the estimated incidences of Parkinson’s disease by age, gender, and ethnicity as well as the organismal aspect. The diagnosed Parkinson’s cases through 1994 and1995 were identified amongst members of the Kaiser Permanente Medical Care Program. Kaiser is one of the most credible and variant largest health maintenance organizations in California. Each case of Parkinson’s was subjected to modified standardized criteria/Hughes diagnostic criteria as applied by a movement disorder specialist. The Parkinson’s disease rate per 100,000 person/years was calculated using the Kaiser Permanente member’s information as the common denominator, adjusted for age and gender using the method of standardization. Of the 588 newly diagnosed cases of Parkinson’s disease identified, allowing for an overall age and gender adjusted occurrence rate of 13.4 per 100,000. These occurrences increased beyond the age of 60, with only 4% of the cases being under the age of 50 years. The rate for men was 19.0 per 100,000; the rate for women was lower and concluded to be 9.9 per 100,000.
The same evolution age adjusted rate was highest among Latinos at 16.7 per 1000,000. The second highest rate was followed by non-Hispanic Whites at 13.6 per 100,000 followed by Asians of 11.3 per 100,000. The African American community was least likely at 10.2 per 100,000. This reporting strongly suggests that the incidence of Parkinson’s disease varies by race, age and ethnicity.
The isolation and identity of the single gene mutations that lead to Parkinson's Disease has provided convincing motivation for the use of animals to study normal functions of these Parkinson’s genes and their cellular defects. The mutation related drosophila has shown itself as an effective replica in related gene studies. The equally significant awareness into the cellular basis of Parkinson’s Disease pathogenesis include the revelation that two Parkinson’s Disease genes, PINK1 and parkin, function in a like minded pathway, with PINK1 completely regulating parkin and controlling mitochondrial veracity. This act is completed through the parameters of mitochondrial fission or fusion. Following performances in both