About this Research Topic
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This Research Topic article collection focuses on Altered activity in networks associated with Parkinson's Disease. Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder after Alzheimer's disease and is characterized by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Although its clinical diagnosis is typically based on the development of motor symptoms (e.g., tremor, bradykinesia, rigidity), PD is a complex disorder characterized by numerous motor, cognitive, behavioral, and autonomic symptoms that often manifest in the preclinical stage.
While the patterns of neurodegeneration and accumulation of Lewy bodies directly drive PD symptoms, research is increasingly uncovering the role of aberrant neuronal activity in the cortex and subcortical regions in PD. Specifically, neuroimaging studies observed that the loss of dopamine is associated with widespread anti-homeostatic changes in the connectivity of frontal, sensorimotor, and visual areas. Research is increasingly uncovering that, rather than being adaptive, this compensatory “rewiring” of the brain might sustain the manifestation and progression of motor and non-motor symptoms in PD. Furthermore, L-DOPA treatment is also responsible by itself for maladaptive plasticity processes that might cause the onset of additional symptoms, including levodopa-induced dyskinesias, psychosis, and behavioral changes.
As new and improved theoretical/mathematical approaches to the study of brain connectivity patterns in vivo are developed (e.g., graph analysis), understanding how plasticity mechanisms regulate network activity in response to the progressive loss of dopaminergic neurons and administered treatments might inform about the role of structural and functional networks in PD symptomatology. At the same time, the investigation of the changes in the brain architecture following therapeutic interventions aimed at reducing PD symptoms can be used as network-based biomarkers of treatment efficacy and response.
This Research Topic aims to gather a comprehensive body of research that would foster our understanding of the architecture and plasticity of resting-state and task-based brain networks in Parkinson’s disease, with the ultimate goal of providing reliable biomarkers of the disorder and guiding future intervention to reduce the symptomatology and progression of the disease.
Furthermore, we welcome investigations on the effects of currently available pharmacological, invasive (i.e., Deep Brain Stimulation - DBS) and non-invasive brain stimulation techniques (e.g., repetitive Transcranial Magnetic Stimulation -rTMS), and behavioral interventions (e.g., motor exercise) in promoting adaptive changes in the brain organization, reducing disease and/or treatment-induced malaplasticity, and, thus addressing PD symptoms.
While any original research and review article on based neuroimaging techniques (e.g., fMRI, EEG, MEG, NIRS) is welcome, studies focusing on the following areas are particularly of interest:
- Circuit mechanisms behind the motor and non-motor symptoms in PD
- Functional connectivity studies on the development of maladaptive plasticity with PD progression and pharmacological treatments (i.e., Levodopa).
- Effects of treatments with Deep Brain Stimulation (DBS), non-invasive brain stimulation techniques (e.g., repetitive Transcranial Magnetic Stimulation -rTMS), and behavioral interventions (e.g., motor exercise, art therapy) on the functional organization of brain networks.
- Simultaneous recordings from scalp EEG and externalized DBS electrodes and connectivity strength between EEG sensors and deep electrodes in PD.
- The use of connectivity measures as a diagnostic tool for PD and atypical parkinsonian disorders.
- Studies on cortical-subcortical connectivity by the use of implantable deep brain stimulation devices and the simultaneous chronic electrophysiological (LFP-EEG) recording and stimulation.
- The use of connectivity measures as prognostic biomarkers of the outcome of the available treatments.
Keywords: Parkinson’s disease, networks, connectomics, functional connectivity, plasticity
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