Parkinson’s disease is the second more common progressive neurodegenerative disorder and it affects both motor and non-motor functions. Bradykinesia, stiffness, and tremor are among the symptoms caused by the loss of dopaminergic neurons in the substantia nigra. In addition to these well-known motor abnormalities, the disease also manifests a variety of non-motor symptoms, such as autonomic dysfunction and REM sleep disorders, which frequently manifest well before the traditional clinical findings. Structural MRI analysis, along with genetic expression mapping, provides a method for better understanding the mechanisms driving neurodegeneration in Parkinson's disease. By examining brainstem regions implicated in the disease, it is possible to identify patterns of atrophy and molecular changes that may serve as early biomarkers. The volumetric changes in brainstem structures have been evaluated using brain imaging data from large-scale observational study. Gene expression patterns in these same regions were identified via post-mortem transcriptomic data. Results suggest that people with Parkinson's disease have severe structural degradation in specific brainstem locations, with certain nuclei exhibiting high correlations with motor disability. Furthermore, areas associated with the regulation of REM sleep seem to experience unique atrophy patterns, which supports their involvement in the prodromal stage of the illness. These directly impacted regions may share transcriptional commonalities, according to gene expression analysis, indicating possible biological processes underlying neurodegeneration. By integrating neuroimaging with transcriptomics, it becomes possible to move toward a biomarker-based approach to Parkinson’s disease. This combination of techniques advances our knowledge of the pathophysiology of the illness, providing fresh avenues for future investigation and possible treatment approaches.

Parkinson’s disease is the second more common progressive neurodegenerative disorder and it affects both motor and non-motor functions. Bradykinesia, stiffness, and tremor are among the symptoms caused by the loss of dopaminergic neurons in the substantia nigra. In addition to these well-known motor abnormalities, the disease also manifests a variety of non-motor symptoms, such as autonomic dysfunction and REM sleep disorders, which frequently manifest well before the traditional clinical findings. Structural MRI analysis, along with genetic expression mapping, provides a method for better understanding the mechanisms driving neurodegeneration in Parkinson's disease. By examining brainstem regions implicated in the disease, it is possible to identify patterns of atrophy and molecular changes that may serve as early biomarkers. The volumetric changes in brainstem structures have been evaluated using brain imaging data from large-scale observational study. Gene expression patterns in these same regions were identified via post-mortem transcriptomic data. Results suggest that people with Parkinson's disease have severe structural degradation in specific brainstem locations, with certain nuclei exhibiting high correlations with motor disability. Furthermore, areas associated with the regulation of REM sleep seem to experience unique atrophy patterns, which supports their involvement in the prodromal stage of the illness. These directly impacted regions may share transcriptional commonalities, according to gene expression analysis, indicating possible biological processes underlying neurodegeneration. By integrating neuroimaging with transcriptomics, it becomes possible to move toward a biomarker-based approach to Parkinson’s disease. This combination of techniques advances our knowledge of the pathophysiology of the illness, providing fresh avenues for future investigation and possible treatment approaches.

Identification of Biomarkers for Parkinson's Disease through Structural MRI Analysis and Genetic Expression Mapping

TAMBA, CARLO
2023/2024

Abstract

Parkinson’s disease is the second more common progressive neurodegenerative disorder and it affects both motor and non-motor functions. Bradykinesia, stiffness, and tremor are among the symptoms caused by the loss of dopaminergic neurons in the substantia nigra. In addition to these well-known motor abnormalities, the disease also manifests a variety of non-motor symptoms, such as autonomic dysfunction and REM sleep disorders, which frequently manifest well before the traditional clinical findings. Structural MRI analysis, along with genetic expression mapping, provides a method for better understanding the mechanisms driving neurodegeneration in Parkinson's disease. By examining brainstem regions implicated in the disease, it is possible to identify patterns of atrophy and molecular changes that may serve as early biomarkers. The volumetric changes in brainstem structures have been evaluated using brain imaging data from large-scale observational study. Gene expression patterns in these same regions were identified via post-mortem transcriptomic data. Results suggest that people with Parkinson's disease have severe structural degradation in specific brainstem locations, with certain nuclei exhibiting high correlations with motor disability. Furthermore, areas associated with the regulation of REM sleep seem to experience unique atrophy patterns, which supports their involvement in the prodromal stage of the illness. These directly impacted regions may share transcriptional commonalities, according to gene expression analysis, indicating possible biological processes underlying neurodegeneration. By integrating neuroimaging with transcriptomics, it becomes possible to move toward a biomarker-based approach to Parkinson’s disease. This combination of techniques advances our knowledge of the pathophysiology of the illness, providing fresh avenues for future investigation and possible treatment approaches.
Identification of Biomarkers for Parkinson's Disease through Structural MRI Analysis and Genetic Expression Mapping
Parkinson’s disease is the second more common progressive neurodegenerative disorder and it affects both motor and non-motor functions. Bradykinesia, stiffness, and tremor are among the symptoms caused by the loss of dopaminergic neurons in the substantia nigra. In addition to these well-known motor abnormalities, the disease also manifests a variety of non-motor symptoms, such as autonomic dysfunction and REM sleep disorders, which frequently manifest well before the traditional clinical findings. Structural MRI analysis, along with genetic expression mapping, provides a method for better understanding the mechanisms driving neurodegeneration in Parkinson's disease. By examining brainstem regions implicated in the disease, it is possible to identify patterns of atrophy and molecular changes that may serve as early biomarkers. The volumetric changes in brainstem structures have been evaluated using brain imaging data from large-scale observational study. Gene expression patterns in these same regions were identified via post-mortem transcriptomic data. Results suggest that people with Parkinson's disease have severe structural degradation in specific brainstem locations, with certain nuclei exhibiting high correlations with motor disability. Furthermore, areas associated with the regulation of REM sleep seem to experience unique atrophy patterns, which supports their involvement in the prodromal stage of the illness. These directly impacted regions may share transcriptional commonalities, according to gene expression analysis, indicating possible biological processes underlying neurodegeneration. By integrating neuroimaging with transcriptomics, it becomes possible to move toward a biomarker-based approach to Parkinson’s disease. This combination of techniques advances our knowledge of the pathophysiology of the illness, providing fresh avenues for future investigation and possible treatment approaches.
DI CUNTO, FERDINANDO
Non autorizzo consultazione esterna dell'elaborato
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14240/163688