Parkinson’s Disease (PD) is a neurodegenerative disorder with unclear etiology. Neuroinflammation pathways, especially linked to NLRP3 inflammasome and Interferon-γ/Interferon-β signaling, is emerging to be an important factor in the upset and progression of the disease. Microglia are the resident immune cells in the brain, triggering neuroinflammatory response upon any detection of signs for brain lesions or nervous system dysfunction. A misregulated microglia response could lead to chronic activation and cause the loss of dopaminergic neurons which is typical of PD. From an evolutionary perspective, microglia appear as a novelty, lacking in Invertebrates, and show interspecific variability in their physiology. In the present study, we aim at studying neuroinflammatory response in both mouse and human microglia, even in association with the PD-linked mutation G2019S on LRRK2 gene.

Parkinson’s Disease (PD) is a neurodegenerative disorder with unclear etiology. Neuroinflammation pathways, especially linked to NLRP3 inflammasome and Interferon-γ/Interferon-β signaling, is emerging to be an important factor in the upset and progression of the disease. Microglia are the resident immune cells in the brain, triggering neuroinflammatory response upon any detection of signs for brain lesions or nervous system dysfunction. A misregulated microglia response could lead to chronic activation and cause the loss of dopaminergic neurons which is typical of PD. From an evolutionary perspective, microglia appear as a novelty, lacking in Invertebrates, and show interspecific variability in their physiology. In the present study, we aim at studying neuroinflammatory response in both mouse and human microglia, even in association with the PD-linked mutation G2019S on LRRK2 gene.

NLRP3 inflammasome activation in primary murine microglia and monocyte-derived human microglia

BARATTA, THOMAS
2022/2023

Abstract

Parkinson’s Disease (PD) is a neurodegenerative disorder with unclear etiology. Neuroinflammation pathways, especially linked to NLRP3 inflammasome and Interferon-γ/Interferon-β signaling, is emerging to be an important factor in the upset and progression of the disease. Microglia are the resident immune cells in the brain, triggering neuroinflammatory response upon any detection of signs for brain lesions or nervous system dysfunction. A misregulated microglia response could lead to chronic activation and cause the loss of dopaminergic neurons which is typical of PD. From an evolutionary perspective, microglia appear as a novelty, lacking in Invertebrates, and show interspecific variability in their physiology. In the present study, we aim at studying neuroinflammatory response in both mouse and human microglia, even in association with the PD-linked mutation G2019S on LRRK2 gene.
2022
NLRP3 inflammasome activation in primary murine microglia and monocyte-derived human microglia
Parkinson’s Disease (PD) is a neurodegenerative disorder with unclear etiology. Neuroinflammation pathways, especially linked to NLRP3 inflammasome and Interferon-γ/Interferon-β signaling, is emerging to be an important factor in the upset and progression of the disease. Microglia are the resident immune cells in the brain, triggering neuroinflammatory response upon any detection of signs for brain lesions or nervous system dysfunction. A misregulated microglia response could lead to chronic activation and cause the loss of dopaminergic neurons which is typical of PD. From an evolutionary perspective, microglia appear as a novelty, lacking in Invertebrates, and show interspecific variability in their physiology. In the present study, we aim at studying neuroinflammatory response in both mouse and human microglia, even in association with the PD-linked mutation G2019S on LRRK2 gene.
Parkinson's Disease
Neuroinflammation
NLRP3
LRRK2
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12608/52346