How does aerobic exercise impact motor symptom progression in individuals with Parkinson’s disease?

How does aerobic exercise impact motor symptom progression in individuals with Parkinson’s disease?

1134 755 Maggie Ford, MD

Previous studies have shown that physical exercise can improve motor symptoms in Parkinson’s disease (PD).1,2 In a recent single-centre, prospective, Phase 2, double-blind, randomised, placebo-controlled trial called Park-in-Shape, Van der Kolk et al. studied the effect of aerobic exercise in 130 individuals with PD.1 The authors found that aerobic exercise slowed the progression of motor symptoms.1 However, all of the exact mechanisms of how aerobic exercise attenuates motor symptom progression are not yet fully understood.3 It is known that there is dopamine depletion in the striatum of individuals with PD.4 This depletion leads to impairments in movement and cognition, due to dysfunction in the corticostriatal networks.4 Furthermore, resting-state functional magnetic resonance imaging (MRI) of individuals with PD has shown alterations in corticostriatal functional connectivity, such that there is a greater dependence on the anterior putamen.5 In healthy individuals the opposite is observed: corticostriatal sensorimotor regions normally show connectivity with the posterior putamen.5 Perhaps aerobic exercise boosts adaptive neuroplasticity in the striatum, positively affecting clinical disease progression of motor symptoms in individuals with PD.3

 

More from the Park-in-Shape trial

As a follow-up to the Park-in-Shape trial, the authors further explored the relationship between aerobic exercise and changes in disease-related brain function and structure by utilising brain imaging in a second study.3 The authors, Johansson et al., wanted to examine whether aerobic exercise altered the balance of corticostriatal sensorimotor connectivity in PD, shifting the balance from the posterior putamen towards the anterior putamen.3 For this second study, the authors used an unselected subset of 57 individuals from the Park-in-Shape trial. Twenty-five individuals who had been previously randomised to home-based aerobic exercise and 31 individuals who had been previously randomised to the home-based active control underwent resting-state functional and structural MRI, and oculomotor cognitive control tasks at baseline and at a 6-month follow-up.3 The study assessments took place in the Netherlands at the Donders Centre for Neuroimaging in Nijmegen between January 20, 2016 and June 1, 2018.3

 

Corticostriatal sensorimotor network and brain structure and the effect of aerobic exercise

Johansson et al. found that compared to individuals randomised to the active control, individuals randomised to aerobic biking exercise had a significantly higher posterior-to-anterior shift in corticostriatal sensorimotor connectivity.3 Moreover, in the aerobic exercise group, functional connectivity increased in the anterior putamen, specifically in the right primary motor cortex, primary somatosensory cortex and the premotor cortex.3 Aerobic exercise was also found to significantly reduce global brain atrophy (P=0.049).3 The substantia nigra tissue integrity and the localised grey matter volume were not affected by aerobic exercise.3 Lastly, antisaccade error rates were decreased while prosaccade amplitudes were increased in the intervention group, suggesting improved cognitive control.3

 

Aerobic exercise is a non-pharmacological treatment option that can improve motor symptoms

Aerobic exercise results in structural and functional changes in the brains of individuals with PD.3 These findings, combined with the positive clinical results from the initial Park-in-Shape trial,1 indicate that aerobic exercise attenuates motor symptom progression and improves cognition by stimulating neuroplasticity in the corticostriatal sensorimotor and cognitive control networks in individuals with PD.3


References
  1. van der Kolk NM et al. BMC Neurol. 2015;15:56.
  2. Schenkman M et al. JAMA Neurol. 2018;75(2):219–226.
  3. Johansson ME et al. Ann Neurol. 2022;91(2):203–216.
  4. Redgrave P et al. Nat Rev Neurosci. 2010;11(11):760–772.
  5. Helmich RC et al. Cereb Cortex. 2010;20(5):1175–1186.

 

Brainwork is supported by unrestricted grants from: