This is an impressive study in terms of the very long follow-up data in a highly selected group of three young-onset PD patients. Collecting detailed clinical and imaging data on patients after an intervention 13 to 16 years earlier is a significant task. It is remarkable that these three individuals continued to get improvement in their PD motor symptoms from the transplants after so many years and they continued not to require any levodopa medication. However, these individuals developed increasing difficulties with the non-motor features of PD.

We need to keep in mind these were very young patients whose disease started at ~34 years old. This is rare in PD. None of them had developed a dementia after more than 25 years of disease, which would not be typical for most PD individuals. This is often the most disabling non-motor feature of PD. Although the PD control group was matched for current age, the difference in disease duration between them was 20 years and so the comparisons made between the groups need to be interpreted with caution.

The authors try to link the...  Read more

This is an impressive study in terms of the very long follow-up data in a highly selected group of three young-onset PD patients. Collecting detailed clinical and imaging data on patients after an intervention 13 to 16 years earlier is a significant task. It is remarkable that these three individuals continued to get improvement in their PD motor symptoms from the transplants after so many years and they continued not to require any levodopa medication. However, these individuals developed increasing difficulties with the non-motor features of PD.

We need to keep in mind these were very young patients whose disease started at ~34 years old. This is rare in PD. None of them had developed a dementia after more than 25 years of disease, which would not be typical for most PD individuals. This is often the most disabling non-motor feature of PD. Although the PD control group was matched for current age, the difference in disease duration between them was 20 years and so the comparisons made between the groups need to be interpreted with caution.

The authors try to link the non-motor symptoms of these three grafted PD individuals to their low serotonergic levels as measured by DASB PET scans. Their final comment that one might consider trying to transplant serotonergic cells to replace this deficit will be met with great skepticism by most researchers. It is clear that a wide range of cells degenerate in more advanced PD. Targeting just one of these non-dopamine cell types is unlikely to reverse the many problems of advanced PD.

We have a wide variety of treatment options that currently control the motor symptoms for most PD patients. Clearly we need to understand the overall degenerative process better before we can consider future dopaminergic AND non-dopaminergic transplantation techniques.

View all comments by David Grimes