Basically, he's saying, So let's get on with it! We need to study other things. I have gisted some of the medicalese in brackets to make it more comfortable to read.

Jaye

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Neurology. 2007 Oct 23;69(17):1701-11. Links
Beating a dead horse: dopamine and Parkinson disease.

Ahlskog JE.
Department of Neurology, Mayo Clinic

Our collective thinking about Parkinson disease (PD) has been heavily influenced by the dramatic response to dopamine replacement therapy. For progress to continue, however, we need to take a broad view of this disorder, which includes recognition of the following. First, substantial evidence now indicates that dopamine oxidation is unlikely to substantially contribute to the pathogenesis of PD [means roughly that the body's processing dopamine probably doesn't hurt you much]. Second, levodopa therapy is not associated with neurotoxicity [it doesn't damage the brain or nerve cells]. Third, the first neurons affected in PD are nondopaminergic [PD starts first in other places than the substantia nigra layer of the brain, where the dopamine-making cells are]; the substantia nigra and other dopaminergic nuclei are affected only later in the course. Thus, PD is much more than degeneration of the dopaminergic nigrostriatal system. Fourth, in the current era, most of the disability of advancing PD is from involvement of nondopaminergic [non-dopamine-making] systems, including levodopa-refractory motor symptoms, dementia, and dysautonomia [dyskinesia, dystonia, dementia, malfunction of the autonomic nervous system]. Motor complications associated with levodopa therapy can be problematic, but they can be controlled in most, using available medications and deep brain stimulation surgery. We have reached the point of diminishing therapeutic returns with drugs acting on dopamine systems; more dopaminergic medications will provide only modest incremental benefit over current therapies. Finally, the benefits from transplantation surgeries aimed at restoring dopaminergic neurotransmission will be limited because later-stage PD disability comes from nondopaminergic substrates. Scale.
PMID: 17954785 [PubMed - in process]

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