Parkinson's disease (PD) is a progressive nervous system disorder that affects movement, and is recognized as the second most prevalent neurodegenerative disease. Clinically, PD is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta, with the pathological hallmark of intracellular a-synuclein aggregates in Lewy bodies and Lewy neurites. Additionally, several processes have been implicated in PD, including mitochondrial dysfunction, protein clearance deficiency, and neuroinflammation, however, the way in which these factors interact remains incompletely understood. In the last decade, the booming of the transcriptomic studies shed light on gene expression profiles at molecular levels, providing insight for mechanistic targets of the degenerative nervous system. What's more, the recent developed antibodies and small molecules targeting a-synuclein aggregation, antisense oligonucleotides, and PROTAC-assisted protein degradation systems are emerging as potential therapeutic interventions for the treatment of synucleinopathies, such as PD, dementia with Lewy Body, and multiple system atrophy.
This Research Topic is dedicated to understanding the crucial roles of a-synuclein in the pathophysiological processes in PD as well as its related synucleinopathies. In addition, the emerging novel therapeutic strategies are also expected to guide the prevention, diagnosis, and treatment of neurological disorders.
We welcome all submissions in the form of Perspectives, Methods, Brief research report, Original Research or Reviews including, but not limited to:
• Investigate the synaptic release and functions of a-synuclein under physiological conditions;
• Identify key regulatory genetics or non-genetics factors (environmental factors) in the development of neuroinflammation and neuropathology of PD;
• Investigate a-synuclein aggregation, secretion and spreading between neurons and glial cells under neurodegenerative and neuroinflammatory conditions;
• Use innovative approaches to analyze the functional and structural heterogeneity of pathological a-synuclein “seeds” among PD, DLB and MSA;
• Explore the recently developed novel therapeutic strategies in the neuroprotection and neurorestoration of PD;
• Establish novel approaches or disease-modeling systems to study the pathogenesis or diagnosis of a-synuclein-related neurological disorders.
Parkinson's disease (PD) is a progressive nervous system disorder that affects movement, and is recognized as the second most prevalent neurodegenerative disease. Clinically, PD is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta, with the pathological hallmark of intracellular a-synuclein aggregates in Lewy bodies and Lewy neurites. Additionally, several processes have been implicated in PD, including mitochondrial dysfunction, protein clearance deficiency, and neuroinflammation, however, the way in which these factors interact remains incompletely understood. In the last decade, the booming of the transcriptomic studies shed light on gene expression profiles at molecular levels, providing insight for mechanistic targets of the degenerative nervous system. What's more, the recent developed antibodies and small molecules targeting a-synuclein aggregation, antisense oligonucleotides, and PROTAC-assisted protein degradation systems are emerging as potential therapeutic interventions for the treatment of synucleinopathies, such as PD, dementia with Lewy Body, and multiple system atrophy.
This Research Topic is dedicated to understanding the crucial roles of a-synuclein in the pathophysiological processes in PD as well as its related synucleinopathies. In addition, the emerging novel therapeutic strategies are also expected to guide the prevention, diagnosis, and treatment of neurological disorders.
We welcome all submissions in the form of Perspectives, Methods, Brief research report, Original Research or Reviews including, but not limited to:
• Investigate the synaptic release and functions of a-synuclein under physiological conditions;
• Identify key regulatory genetics or non-genetics factors (environmental factors) in the development of neuroinflammation and neuropathology of PD;
• Investigate a-synuclein aggregation, secretion and spreading between neurons and glial cells under neurodegenerative and neuroinflammatory conditions;
• Use innovative approaches to analyze the functional and structural heterogeneity of pathological a-synuclein “seeds” among PD, DLB and MSA;
• Explore the recently developed novel therapeutic strategies in the neuroprotection and neurorestoration of PD;
• Establish novel approaches or disease-modeling systems to study the pathogenesis or diagnosis of a-synuclein-related neurological disorders.
