Abstract
The recent application of graph theory to brain networks promises to shed light on complex diseases such as Parkinson’s disease (PD). This study aimed to investigate functional changes in sensorimotor and cognitive networks in Parkinsonian patients, with a focus on inter- and intra-connectivity organization in the disease-associated nodal and hub regions using the graph theoretical analyses. Resting-state functional MRI data of a total of 65 participants, including 23 healthy controls (HCs) and 42 patients, were investigated in 120 nodes for local efficiency, betweenness centrality, and degree. Hub regions were identified in the HC and patient groups. We found nodal and hub changes in patients compared with HCs, including the right pre-supplementary motor area (SMA), left anterior insula, bilateral mid-insula, bilateral dorsolateral prefrontal cortex (DLPFC), and right caudate nucleus. In general, nodal regions within the sensorimotor network (i.e., right pre-SMA and right mid-insula) displayed weakened connectivity, with the former node associated with more severe bradykinesia, and impaired integration with default mode network regions. The left mid-insula also lost its hub properties in patients. Within the executive networks, the left anterior insular cortex lost its hub properties in patients, while a new hub region was identified in the right caudate nucleus, paralleled by an increased level of inter- and intra-connectivity in the bilateral DLPFC possibly representing compensatory mechanisms. These findings highlight the diffuse changes in nodal organization and regional hub disruption accounting for the distributed abnormalities across brain networks and the clinical manifestations of PD.
Highlights
The clinical phenotypes of Parkinson’s disease (PD) include cardinal motor symptoms such as tremor, rigidity, bradykinesia, and loss of postural stability, along with a set of nonmotor symptoms such as depression, sleep disturbances, autonomic dysfunction and cognitive impairment (Barnum and Tansey, 2012; Bonnet et al, 2012)
We found nodal and hub changes in patients compared with healthy controls (HCs), including the right pre-supplementary motor area (SMA), left anterior insula, bilateral mid-insula, bilateral dorsolateral prefrontal cortex (DLPFC), and right caudate nucleus
Cognitive impairment is one of the Network Changes in Parkinson’s Disease most common non-motor symptoms in PD. It ranges from mild cognitive impairment in different cognitive domains to dementia, which is thought to be derived from dysfunction of different neurotransmitter systems/brain networks (Gratwicke et al, 2015) associated with Lewy pathology and Alzheimer’s disease pathology in cortical and subcortical regions (Halliday et al, 2014)
Summary
The clinical phenotypes of Parkinson’s disease (PD) include cardinal motor symptoms such as tremor, rigidity, bradykinesia, and loss of postural stability, along with a set of nonmotor symptoms such as depression, sleep disturbances, autonomic dysfunction and cognitive impairment (Barnum and Tansey, 2012; Bonnet et al, 2012). The anterior and posterior cingulate cortices, insula, and superior frontal and parietal cortex are identified as both structural and functional hubs (van den Heuvel and Sporns, 2013; Sporns, 2014). These are heteromodal areas that are involved in a broad range of cognitive processes (Achard et al, 2006). The coexistence and balance of segregation and integration of modules are fundamental for brain function (Bullmore and Sporns, 2012; Sporns, 2013)
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