This is an interesting manuscript that asks whether two different classes of anti-parkinsonian drugs (the dopamine precursor L-DOPA, and the D2/D3 dopamine receptor agonist pramipexole) differentially affect dopamine neuron viability over the course of 4 years, as detected by the SPECT ligand CIT. CIT and other tropane analogs bind to the dopamine transporter, a protein localized almost exclusively on dopamine neurons. The conclusions drawn are that early intervention with pramipexole is more effective than L-DOPA in retarding dopamine neuronal degeneration. The tantalizing conclusions support the view that specific anti-Parkinsonian drugs may "protect" dopamine neurons from further degeneration.

The conclusions require some tempering because, although the transporter is an effective marker of dopamine neurons, it is increasingly recognized that the transporter can be regulated. That is, the transporter may up- and down-regulate and traffic top the interior of the cell in response to substrates and antagonists. Accordingly, it is not clear whether the findings reflect...  Read more

This is an interesting manuscript that asks whether two different classes of anti-parkinsonian drugs (the dopamine precursor L-DOPA, and the D2/D3 dopamine receptor agonist pramipexole) differentially affect dopamine neuron viability over the course of 4 years, as detected by the SPECT ligand CIT. CIT and other tropane analogs bind to the dopamine transporter, a protein localized almost exclusively on dopamine neurons. The conclusions drawn are that early intervention with pramipexole is more effective than L-DOPA in retarding dopamine neuronal degeneration. The tantalizing conclusions support the view that specific anti-Parkinsonian drugs may "protect" dopamine neurons from further degeneration.

The conclusions require some tempering because, although the transporter is an effective marker of dopamine neurons, it is increasingly recognized that the transporter can be regulated. That is, the transporter may up- and down-regulate and traffic top the interior of the cell in response to substrates and antagonists. Accordingly, it is not clear whether the findings reflect neuroprotection or a regulated transporter.

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