Subthalamic and pallidal stimulation in Parkinson's disease induce distinct brain topological reconstruction

Chu, Chunguang; He, Naying; Zeljic, Kristina; Zhang, Zhen; Wang, Jiang; Li, Jun; Liu, Yu; Zhang, Youmin; Sun, Bomin; Li, Dianyou; Yan, Fuhua; Zhang, Chencheng; Liu, Chen

doi:10.1016/j.neuroimage.2022.119196

Cited by 8 publications

(2 citation statements)

References 57 publications

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“…We converted all DICOM files to NifTi format using the SPM12 software ( https://www.fil.ion.ucl.ac.uk/spm/software/spm12/ ) and carefully inspected the data for quality. For data preprocessing and image analysis, we employed the FreeSurfer software (version development, http://www.freesurfer.net ), and GRETNA 2.0.0 toolbox ( https://www.nitrc.org/projects/gretna/ ) as previously described 62 , 63 .…”

Section: Methodsmentioning

confidence: 99%

Acoustic assessment in mandarin-speaking Parkinson’s disease patients and disease progression monitoring and brain impairment within the speech subsystem

Diao,

Xie,

Wang

et al. 2024

npj Parkinsons Dis.

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Approximately 90% of Parkinson’s patients (PD) suffer from dysarthria. However, there is currently a lack of research on acoustic measurements and speech impairment patterns among Mandarin-speaking individuals with PD. This study aims to assess the diagnosis and disease monitoring possibility in Mandarin-speaking PD patients through the recommended speech paradigm for non-tonal languages, and to explore the anatomical and functional substrates. We examined total of 160 native Mandarin-speaking Chinese participants consisting of 80 PD patients, 40 healthy controls (HC), and 40 MRI controls. We screened the optimal acoustic metric combination for PD diagnosis. Finally, we used the objective metrics to predict the patient’s motor status using the Naïve Bayes model and analyzed the correlations between cortical thickness, subcortical volumes, functional connectivity, and network properties. Comprehensive acoustic screening based on prosodic, articulation, and phonation abnormalities allows differentiation between HC and PD with an area under the curve of 0.931. Patients with slowed reading exhibited atrophy of the fusiform gyrus (FDR p = 0.010, R = 0.391), reduced functional connectivity between the fusiform gyrus and motor cortex, and increased nodal local efficiency (NLE) and nodal efficiency (NE) in bilateral pallidum. Patients with prolonged pauses demonstrated atrophy in the left hippocampus, along with decreased NLE and NE. The acoustic assessment in Mandarin proves effective in diagnosis and disease monitoring for Mandarin-speaking PD patients, generalizing standardized acoustic guidelines beyond non-tonal languages. The speech impairment in Mandarin-speaking PD patients not only involves motor aspects of speech but also encompasses the cognitive processes underlying language generation.

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Section: Methodsmentioning

confidence: 99%

Acoustic assessment in mandarin-speaking Parkinson’s disease patients and disease progression monitoring and brain impairment within the speech subsystem

Diao,

Xie,

Wang

et al. 2024

npj Parkinsons Dis.

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“…Studies in DJ-1 knockout (KO) mice and cells showed impaired complex-I-dependent respiration, and DJ-1 KO produced changes in mitochondrial morphology that were linked to mitochondrial ROS production and impaired respiration [55,56]. This impairment could decrease the energy outcome of cell metabolism, which is especially problematic for dopaminergic neurons that require high amounts of energy due to their axonal connections with other areas involved in movement and motor control [57][58][59]. Humans carrying the homozygote E64D mutation in DJ-1 showed the same dysfunctional mitochondrial phenotype as in DJ-1 KO mice, indicating that DJ-1 plays a crucial role in conserving mitochondrial morphology in PD [55].…”

Section: Role Of Dj-1 In Mitochondrial Homeostasismentioning

confidence: 99%

Pathogenesis of DJ-1/PARK7-Mediated Parkinson’s Disease

Skou,

Johansen,

Okarmus

et al. 2024

Cells

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Parkinson’s disease (PD) is a common movement disorder associated with the degeneration of dopaminergic neurons in the substantia nigra pars compacta. Mutations in the PD-associated gene PARK7 alter the structure and function of the encoded protein DJ-1, and the resulting autosomal recessively inherited disease increases the risk of developing PD. DJ-1 was first discovered in 1997 as an oncogene and was associated with early-onset PD in 2003. Mutations in DJ-1 account for approximately 1% of all recessively inherited early-onset PD occurrences, and the functions of the protein have been studied extensively. In healthy subjects, DJ-1 acts as an antioxidant and oxidative stress sensor in several neuroprotective mechanisms. It is also involved in mitochondrial homeostasis, regulation of apoptosis, chaperone-mediated autophagy (CMA), and dopamine homeostasis by regulating various signaling pathways, transcription factors, and molecular chaperone functions. While DJ-1 protects neurons against damaging reactive oxygen species, neurotoxins, and mutant α-synuclein, mutations in the protein may lead to inefficient neuroprotection and the progression of PD. As current therapies treat only the symptoms of PD, the development of therapies that directly inhibit oxidative stress-induced neuronal cell death is critical. DJ-1 has been proposed as a potential therapeutic target, while oxidized DJ-1 could operate as a biomarker for PD. In this paper, we review the role of DJ-1 in the pathogenesis of PD by highlighting some of its key neuroprotective functions and the consequences of its dysfunction.

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Multimodal neuroimaging to characterize symptom-specific networks in movement disorders

Ellis,

Meyer,

Kaasinen

et al. 2024

npj Parkinsons Dis.

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Movement disorders, such as Parkinson’s disease, essential tremor, and dystonia, are characterized by their predominant motor symptoms, yet diseases causing abnormal movement also encompass several other symptoms, including non-motor symptoms. Here we review recent advances from studies of brain lesions, neuroimaging, and neuromodulation that provide converging evidence on symptom-specific brain networks in movement disorders. Although movement disorders have traditionally been conceptualized as disorders of the basal ganglia, cumulative data from brain lesions causing parkinsonism, tremor and dystonia have now demonstrated that this view is incomplete. Several recent studies have shown that lesions causing a given movement disorder occur in heterogeneous brain locations, but disrupt common brain networks, which appear to be specific to each motor phenotype. In addition, findings from structural and functional neuroimaging in movement disorders have demonstrated that brain abnormalities extend far beyond the brain networks associated with the motor symptoms. In fact, neuroimaging findings in each movement disorder are strongly influenced by the constellation of patients’ symptoms that also seem to map to specific networks rather than individual anatomical structures or single neurotransmitters. Finally, observations from deep brain stimulation have demonstrated that clinical changes, including both symptom improvement and side effects, are dependent on the modulation of large-scale networks instead of purely local effects of the neuromodulation. Combined, this multimodal evidence suggests that symptoms in movement disorders arise from distinct brain networks, encouraging multimodal imaging studies to better characterize the underlying symptom-specific mechanisms and individually tailor treatment approaches.

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Subthalamic and pallidal stimulation in Parkinson's disease induce distinct brain topological reconstruction

Cited by 8 publications

References 57 publications

Acoustic assessment in mandarin-speaking Parkinson’s disease patients and disease progression monitoring and brain impairment within the speech subsystem

Acoustic assessment in mandarin-speaking Parkinson’s disease patients and disease progression monitoring and brain impairment within the speech subsystem

Pathogenesis of DJ-1/PARK7-Mediated Parkinson’s Disease

Multimodal neuroimaging to characterize symptom-specific networks in movement disorders

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