In Reply: Dr Ahlskog and colleagues, Dr Albin
and colleagues, and Dr Moorish advise caution in interpreting the relative
reduction in the loss of striatal β-CIT uptake from baseline in patients
with early PD after initial treatment with pramipexole vs levodopa. We agree
entirely that our data do not demonstrate either that pramipexole is neuroprotective
or that levodopa is neurotoxic in patients with PD. Ahlskog et al and Albin
et al focus on the possibility that either pramipexole or levodopa may alter
DAT imaging via a pharmacologic effect. Current data argue against these explanations
of our results. Indirect evidence comes from a recent study demonstrating
a relative reduction in the loss of 18F-dopa uptake after 2 years
of treatment with ropinirole (a dopamine agonist like pramipexole) vs levodopa1 of similar magnitude to the relative reduction
in loss of β-CIT uptake in the pramipexole group in our study. This strongly
suggests that our observed treatment effects are not explained by acute effects
on DAT binding.
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