Does Aerobic exercise alter brain function and structure in Parkinson’s disease? What you need to know about the new Dutch study
A Dutch group recently completed a clinical trial called the Park-in-Shape. The authors then took a small subset of folks from the original trial and completed a second study on how Aerobic Exercise Alters Brain Function and Structure in Parkinson’s Disease. We will summarize some of the major findings from this study.
What did the authors actually do in this study?
Was this part of the Park-in-Shape study?
Park-in-Shape was a single-center, double-blind randomized controlled trial in 130 persons with Parkinson’s disease (who were considered sedentary)
In the original trial folks were randomly assigned to aerobic exercise (stationary home trainer) or stretching (active control). The study was conducted over 6 months.
The exercise group had 35 and the stretching group 31 participants.
They had all participants consent to obtaining resting-state functional and structural magnetic resonance imaging (MRI), and an eye baaed cognitive control task.
They compared baseline to 6 month outcomes.
What did the author’s think were the therapeutic
implications?
The authors were fair in their assessment that “achieving any lasting restoration of function in this network may be difficult, given the extent of nigrostriatal cell loss that is already present at clinical onset.”
They suggest an alternative “to influence clinical decline may be to focus on maintaining corticostriatal sensorimotor function against disease progression and to strengthen compensatory cognitive processes.”
They also caution that “connectivity brain changes and motor symptom progression are highly complex measurements that aggregate multiple domains (eg, functional specialization of brain regions and subsets of symptoms at the clinical level). These measurements may not map onto each other in a linear fashion.
What did the author’s conclude?
Aerobic exercise, but not stretching on the advanced imaging tests showed increased functional connectivity of an area of the brain called the anterior putamen which seemed to be connected with the sensorimotor cortex more than a different mostly motor based structure called the posterior putamen.
The exercise group had improved cognitive control.
The exercise group showed increased connectivity in the right fronto-parietal network, and this was directly related to fitness improvements.
The exercise group showed reductions in global brain atrophy (brain shrinkage).
Was exercise truly “neuroprotective” or possibly slow
disease progression?
The answer to this question is debate-able and remains in the eye of the beholder.
It is reasonable to conclude that the MRI, clinical, and behavioral results converged in this small group to suggest aerobic exercise stabilized disease progression over 6 months.
It is reasonable to agree that there were interesting brain network changes.
It is reasonable to conclude there were cognitive benefits.
However, the small size of the study cohort and the lack of changes in the free water imaging marker on MRI would suggest that if exercise is neuroprotective (or impacts disease progression), the effect size is very small.
We are looking forward to larger studies.
To read more books and articles by Michael S. Okun MD check on Twitter @MichaelOkun and these websites with blogs and information on his books and http://parkinsonsecrets.com/ #Livingwith Parkinson’s #EndingPD #Parkinsonsecrets #LessonsFromTheBedside
He also serves as the Medical Advisor for the Parkinson’s Foundation.
To see more on Dr. Indu Subramanian she does live interviews of experts in Parkinson’s for the PMD Alliance.
The blog artist is Jonny Acheson.