Although Parkinson’s disease (PD) is commonly thought to impact gray matter primarily, there is emerging evidence that structural abnormalities in white matter occur. Traditional connectomics tools for studying Parkinson’s disease may not be sensitive to underlying microstructural alterations like myelin atrophy. For a study, researchers sought to determine the changes in myelin content caused by Parkinson’s disease in connections between the basal ganglia and the brainstem. They employed the longitudinal relaxation rate as a physiologically grounded myelin-sensitive measure to weight the connectome.
The myelin-weighted connectome was calculated in 35 healthy control volunteers and 81 Parkinson’s disease patients. To emphasize the disparities between patients with Parkinson’s disease and healthy control participants, they employed partial least squares. Then, on the selected brainstem and subcortical areas, a ring analysis was done to assess each node’s potential involvement as an epicenter for illness progression. Then they utilized behavioral partial least squares to connect myelin changes to clinical ratings.
The majority of connections (~80%) emanating from the basal ganglia have little myelin content. The longitudinal relaxation rate was significantly lower in connections emanating from probable epicentral nodes (substantia nigra, nucleus basalis of Meynert, amygdala, hippocampus, and midbrain) (P<0.05). The impact was not observed in the medulla and pons.
The myelin-weighted connectome was able to detect changes in myelin content in basal ganglia connections in Parkinson’s disease. It might give a distinct perspective on the role of myelination in neurodegeneration and disease development between individuals with Parkinson’s disease and healthy control participants.
Reference:movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mds.28891
