In neurodegenerative diseases, protein aggregation and propagation play an important role in disease progression. Deposition of protein amyloids is the most common feature of neurodegenerative diseases, such as Alzheimer's disease and Parkinson’s disease, but the specific forms of pathological protein aggregation and the exact regulatory mechanisms of protein aggregation remain unclear. Prion-like propagation of various aggregated proteins, including Aß, tau, and a-synuclein, may underlie the progression of pathology in neurodegenerative diseases. The protein propagation undergoes several steps: protein monomer transformation into aggregates, transcellular propagation of aggregated protein, and transmissible neuropathology. Although several independent studies showed that prion-like protein propagation is a common phenomenon, a comprehensive understanding of the regulatory mechanism of prion-like propagation of aggregated protein in neurodegenerative diseases remains to be fully elucidated. Furthermore, we need to investigate the role of glial cells or other cell types in pathogenic protein propagation.
Further investigation into the triggers, facilitators and aggravators of protein aggregation and propagation is crucial for understanding the pathogenesis of neurodegenerative diseases and developing novel therapeutic approaches. For example, exploring the mechanisms underlying the cellular release and uptake of protein aggregates is important for searching therapeutic targets. Understanding the role of free extracellular aggregates is critical for finding diagnostic biomarkers and developing antibody or small molecule therapy.
This research topic aims to collect high-quality reviews, original research articles and perspectives that reveal the roles and mechanisms of protein aggregation and propagation in the pathogenesis of neurodegenerative diseases, with a focus on but not limited to:
- The mechanisms underlying the cellular release and uptake of protein aggregation
- The specific forms of pathological protein aggregation
- The role of glial cells or other cells in the propagation of aggregated protein
- Peripheral aggregated protein as biomarkers
- The role of free extracellular aggregated protein in the pathogenic progression of neurodegenerative diseases, such as Alzheimer's disease and Parkinson’s disease
- The triggers, facilitators and aggravators of aggregated protein propagation
In neurodegenerative diseases, protein aggregation and propagation play an important role in disease progression. Deposition of protein amyloids is the most common feature of neurodegenerative diseases, such as Alzheimer's disease and Parkinson’s disease, but the specific forms of pathological protein aggregation and the exact regulatory mechanisms of protein aggregation remain unclear. Prion-like propagation of various aggregated proteins, including Aß, tau, and a-synuclein, may underlie the progression of pathology in neurodegenerative diseases. The protein propagation undergoes several steps: protein monomer transformation into aggregates, transcellular propagation of aggregated protein, and transmissible neuropathology. Although several independent studies showed that prion-like protein propagation is a common phenomenon, a comprehensive understanding of the regulatory mechanism of prion-like propagation of aggregated protein in neurodegenerative diseases remains to be fully elucidated. Furthermore, we need to investigate the role of glial cells or other cell types in pathogenic protein propagation.
Further investigation into the triggers, facilitators and aggravators of protein aggregation and propagation is crucial for understanding the pathogenesis of neurodegenerative diseases and developing novel therapeutic approaches. For example, exploring the mechanisms underlying the cellular release and uptake of protein aggregates is important for searching therapeutic targets. Understanding the role of free extracellular aggregates is critical for finding diagnostic biomarkers and developing antibody or small molecule therapy.
This research topic aims to collect high-quality reviews, original research articles and perspectives that reveal the roles and mechanisms of protein aggregation and propagation in the pathogenesis of neurodegenerative diseases, with a focus on but not limited to:
- The mechanisms underlying the cellular release and uptake of protein aggregation
- The specific forms of pathological protein aggregation
- The role of glial cells or other cells in the propagation of aggregated protein
- Peripheral aggregated protein as biomarkers
- The role of free extracellular aggregated protein in the pathogenic progression of neurodegenerative diseases, such as Alzheimer's disease and Parkinson’s disease
- The triggers, facilitators and aggravators of aggregated protein propagation
