the ultimate medical object of identifying PD-related genes and their functions in your initial response. That is, to "modulate their activity". Keep in mind that the great majority of cases of PD are not familial or genetically transmitted. Most are so-called "idiopathic" or "sporadic" cases.

To take a couple of examples of types found to be familial;
Alpha synucein was one of the first PD-related genes identified about twelve years ago. It was also found to be a major constituent of Lewey bodies, the microscopic protein aggregates present in the substantia nigra of Parkinson's patients, and which, along with the loss of dopamine-producing neurons in that region, constitutes the only true diagnostic test for the disease. This post-mortem finding is present in both sporadic or familial cases.
Two "point mutations" (single amino acid changes) discovered in synuclein increase the tendency of the affected proteins to form toxic aggregates which eventually form Lewey bodies. Other pateints who do not have alpha synuclein point mutatuons have duplicates or even triplicates of the alpha synuclein gene, causing them to produce an excess of the protein. Still others have genetic alterations which also result in the production of excess synuclein of normal structure without duplication of the gene. This appears to be a result of alterations in so-called "control" gene elements responsible for governing the rate of synthesis of alpha synuclein. So it seems that PD can result from both "crippled" mutant alpha synuclein and an excessive production of the structurally normal protein.
Since there are no known diseases associated with decreased production of alpha synuclein, and mice in which the gene has been experimentally inactivated are healthy, a promising approach to treating either familial or sporadic Parkinson's would be to find a drug that specifically decreases the procuction of alpha synuclein, thus avoiding or delaying its neurotoxic aggregation.

Another more common cause of PD, found most often in familial cases, but occasionally in sporadic ones, is point mutations in the gene for a protein referred to as LRRK2. This protein appears to be an enzyme of the "kinase" family, thus the K in its name. This very large family of enzymes (there are hundreds of different kinases) catalyze the addition of the phosphate group to different molecules. The two most commonly found single-point mutant forms of LRRK2 present in familial PD cases were discovered to have higher enzyme activity than the normal, non-mutant protein. Therefore it would seem that a kinase inhibitor drug specific for this molecule would be a logical approach to this particular form of PD.

My apologies to those who made it this far, but did so with glazed eyes.

Robert