About this Research Topic
Inflammation plays an increasingly recognized and important role in neurodegenerative Parkinson’s disease (PD), with multiple inflammatory processes implicated in risk and progression in both animal models and human tissue. Neuroinflammation in PD is associated with a chronic immune response in the CNS, in which innate immune cells such as astrocytes and microglia are recognized players. However, increasing evidence also indicates that both the innate and the adaptive peripheral immune systems also contribute to PD pathogenesis. Indeed, an integrated peripheral/central immune response likely underlies PD pathogenesis contributing to the hallmark features of PD, namely the accumulation of alpha-synuclein protein and the neurodegeneration, especially the nigral dopaminergic neurons. However, the exact role of inflammation in PD pathogenesis remains to be determined. Moreover, immune processes are suggested to occur very early in disease, even in the prodromal phase. Better understanding of these immune related mechanisms might potentially pave the way for disease modifying treatments that might curtail neurodegeneration.
The goal of this Research Topic is to better elucidate the distinct inflammatory mechanisms in PD and in the prodromal phase of the disease, while providing an updated focused analysis of the current knowledge in the field. To this extent, work on inflammatory mechanisms in both “at risk” populations for PD and subjects diagnosed with PD will be accepted. In addition, interventional trials attempting to modulate neurodegeneration by affecting inflammation or observational trials regarding potential treatment with anti-inflammatory treatments will be welcomed.
As such, Topic Editors will welcome Original Research articles as well as Reviews on, but not limited to the following themes:
1. Prodromal symptoms and inflammation;
2. Glia (astroglia and microglia) response during Parkinson’s disease
3. The role of adaptive and innate immunity in PD;
4. Central vs peripheral inflammation in PD;
5. The contribution of peripheral immune cells to CNS inflammation
6. Evaluation of best modalities to detect inflammation in neurodegeneration;
7. Anti-inflammatory interventions as possible disease modifying treatments in PD.
The goal of this Research Topic is to better elucidate the distinct inflammatory mechanisms in PD and in the prodromal phase of the disease, while providing an updated focused analysis of the current knowledge in the field. To this extent, work on inflammatory mechanisms in both “at risk” populations for PD and subjects diagnosed with PD will be accepted. In addition, interventional trials attempting to modulate neurodegeneration by affecting inflammation or observational trials regarding potential treatment with anti-inflammatory treatments will be welcomed.
As such, Topic Editors will welcome Original Research articles as well as Reviews on, but not limited to the following themes:
1. Prodromal symptoms and inflammation;
2. Glia (astroglia and microglia) response during Parkinson’s disease
3. The role of adaptive and innate immunity in PD;
4. Central vs peripheral inflammation in PD;
5. The contribution of peripheral immune cells to CNS inflammation
6. Evaluation of best modalities to detect inflammation in neurodegeneration;
7. Anti-inflammatory interventions as possible disease modifying treatments in PD.
Keywords: Parkinson's Disease, inflammation, alpha-synuclein, prodromal Parkinson's Disease, astrocytes, microglia, monocytes, T-cell, B-cell, innate immunity, adaptive immunity
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
