Parkinson's disease (PD) is a common age-related neurodegenerative disease affecting 7 to 10 million people worldwide. Alpha-synucleinopathies, including Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy, is a group of illnesses caused by chronic progressive neurodegeneration and loss of dopaminergic neurons in brain. It is a well-accepted fact that the aggregation and transmission of a-synuclein play important roles in the development of a-synucleinopathies. However, the detailed etiology and pathogenesis remain unclear. Uncovering the mechanism of a-synuclein in cellular transmission of Parkinson Disease and other synucleinopathies will be key to identify the disease-prediction biomarkers which are critical for precise diagnosis and therapeutic approaches.
Pre-clinical and clinical investigations encompassing immunology, microbiology, neuroimaging, proteomics and genetics have been conducted in order to clarify the molecular mechanisms and identify useful biomarkers for the disease diagnosis. For instance, studies have shown that immune dysfunction may lead to a-synuclein aggregation and transmission in the brain. Therefore detecting biomarkers in Cerebrospinal Fluid (CSF) or plasma will be helpful to predict the risk and evaluate the progression of PD. Studies also show that changes in gene expression may cause PD, and epigenetic methylation likely plays a significant role in the regulation of gene function. Finally, functional neuroimaging techniques (fMRI) show potential to study the functional connectivity of the brain and the pathophysiology of PD.
This Research Topic aims to generate a multidimensional discussion linking clinical analysis with basic research unveiling the underlying mechanisms of PD. We are particularly interested in studies related to the immune dysfunction which leads to a-synuclein aggregation and transmission, the novel biomarkers for preclinical detection and clinical evaluation, and advanced experimental methods, which will conjointly contribute to a deeper understanding of the disease mechanism thus to better guide the clinical applications.
In this context, we welcome original articles and reviews based on the following sub-themes:
• Clinical investigation about the assessment of new potential biomarkers in blood, saliva, urine and CSF for PD and related movement disorders.
• Clinical research about the molecular imaging to detect the functional brain connectivity for the disease prediction or development.
• Basic research or clinical investigations about the immune dysfunction, microglia reaction and neural inflammation that lead a-synuclein aggregation and transmission in neural cells.
• Basic research about a-synuclein pathology caused by gene dysfunction tested in experiments to disclose the underlying mechanisms of PD and related movement disorders.
Parkinson's disease (PD) is a common age-related neurodegenerative disease affecting 7 to 10 million people worldwide. Alpha-synucleinopathies, including Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy, is a group of illnesses caused by chronic progressive neurodegeneration and loss of dopaminergic neurons in brain. It is a well-accepted fact that the aggregation and transmission of a-synuclein play important roles in the development of a-synucleinopathies. However, the detailed etiology and pathogenesis remain unclear. Uncovering the mechanism of a-synuclein in cellular transmission of Parkinson Disease and other synucleinopathies will be key to identify the disease-prediction biomarkers which are critical for precise diagnosis and therapeutic approaches.
Pre-clinical and clinical investigations encompassing immunology, microbiology, neuroimaging, proteomics and genetics have been conducted in order to clarify the molecular mechanisms and identify useful biomarkers for the disease diagnosis. For instance, studies have shown that immune dysfunction may lead to a-synuclein aggregation and transmission in the brain. Therefore detecting biomarkers in Cerebrospinal Fluid (CSF) or plasma will be helpful to predict the risk and evaluate the progression of PD. Studies also show that changes in gene expression may cause PD, and epigenetic methylation likely plays a significant role in the regulation of gene function. Finally, functional neuroimaging techniques (fMRI) show potential to study the functional connectivity of the brain and the pathophysiology of PD.
This Research Topic aims to generate a multidimensional discussion linking clinical analysis with basic research unveiling the underlying mechanisms of PD. We are particularly interested in studies related to the immune dysfunction which leads to a-synuclein aggregation and transmission, the novel biomarkers for preclinical detection and clinical evaluation, and advanced experimental methods, which will conjointly contribute to a deeper understanding of the disease mechanism thus to better guide the clinical applications.
In this context, we welcome original articles and reviews based on the following sub-themes:
• Clinical investigation about the assessment of new potential biomarkers in blood, saliva, urine and CSF for PD and related movement disorders.
• Clinical research about the molecular imaging to detect the functional brain connectivity for the disease prediction or development.
• Basic research or clinical investigations about the immune dysfunction, microglia reaction and neural inflammation that lead a-synuclein aggregation and transmission in neural cells.
• Basic research about a-synuclein pathology caused by gene dysfunction tested in experiments to disclose the underlying mechanisms of PD and related movement disorders.
