Is that the "plasmid" organelles of a striatal cell have been "transfected" with a gene construct that is incorporated in the plasmid DNA and then expressed as the ability to do three things. The first would be to enzymatically transform phenylalanine into tyrosine, next tyrosine into dopa, then dopa, decarboxylated to dopamine. All needed co-factors for the enzymatic transformations should already be a part of the cellular machinery for similar enzymatic manipulations, albeit, maybe these too need a boost.
My question is, since dopamine production and release from the substantia nigra is the source of striatal dopamine higher in the midbrain, and midbrain dopamine is involved with mood function, not motor function (this is the job of basal ganglia neurons, lower in the brainstem), than what have they accomplished specifically for helping PD?
Since the "dopamine transporter is "compartmentalized" as such, wouldn't the transfection of cells closer to the substantia nigra be the real intent to provide endogenous dopamine that the cells left in the nigral area can exploit?