Lindy, I know. Paula and I chatted about the dopa trap a few times. Her presence is felt - like a guardian angel for this research. I only mean in sense that is has been so understudied compared to dopamine, yet the scarce research I am finding seems to fill in so many holes. This article I am linking, especially in hands of patients, could be a game changer especially when only other thing doc will say is DBS. We all need to read the following article.

I realize that it is more a balance between neurotransmitters; I didn't mean to imply that DA is now not important. However, maybe dopamine is not responsible for movement deficits? How would know otherwise? How can we go for so long primarily focusing on dopamine loss while NA the neurotransmitter that takes the bigger hit is essentially ignored? Point is the reason things are so "off" whether failed clinical trials or our symptoms and med response is that near everything focuses on DA only when in reality it is a package deal. Like you said interdependent.

This article pretty much sums it all up and does answer your question. In animal models of PD, motor dysfunction occurs either only when NA levels are too low or when animal has DA and NA loss but no motor abnormality in loss of only DA. In the original post I link out to a bibliography that includes more on your question.

The good news is this shows there are more treatment options than we thought. The downside is why have not already been developed?

Noradrenaline in Parkinson Disease. Frontiers in Neuroscience. 2011


In the present review, we analyze the latest evidence for the implication of NA in the pathophysiology of PD obtained from animal models of parkinsonism and from parkinsonian patients. Recent studies have shown that NA depletion alone, or combined with DA depletion, results in motor as well as in non-motor dysfunctions. In addition, by using selective agonists and antagonists of noradrenaline alpha receptors we, and others, have shown that α2 receptors are implicated in the control of motor activity and that α2 receptor antagonists can improve PD motor symptoms as well as L-Dopa-induced dyskinesia. In this review we argue that the loss of NA neurons in PD has an impact on all PD symptoms and that the addition of NAergic agents to dopaminergic medication could be beneficial in the treatment of the disease.