Neuroinflammation is currently considered a hallmark of neurodegenerative and neuropsychiatric conditions. Although inflammatory responses mediated by brain immune cells, mainly microglia, are indispensable for tissue homeostasis, overstimulation in the events such as injury and infection may lead to neuronal damage, contributing for the development of neurological morbidities. In this context, accumulating lines of evidence have supported the role of purinergic signalling in neuroinflammation. Upon damage, nucleotides such as ATP, UTP, ADP, UDP, among others, and nucleosides, mainly adenosine, released into the extracellular milieu influence pro- and anti-inflammatory actions. These molecules can bind to their specific purinoceptors, divided into the P1 and P2 families of receptors, expressed on the plasma membrane of cells and mediating a myriad of cellular functions. Nucleotides and nucleosides are eventually degraded by a set of soluble or membrane-bound enzymes, collectively known as ectonucleotidases.
This Research Topic will address some of the main current research on the role of purinergic signaling in neuroinflammation in the events of health and disease conditions. Furthermore, pharmacological targeting of purinergic signaling in distinct scenarios will be a main focus to investigate the landscape of the implications of purinergic system components in the neuroinflammatory responses associated with different pathologies.
Therefore, submission of Original Research, Brief Report, Perspective, Mini-Review, and Review articles focusing on, but not limited to, the following topics are welcome:
• Neuroinflammation, neurodegeneration, neuroregeneration
• Neurodegenerative and neuropsychiatric diseases
• Oxidative/nitrosative stress and neuroinflammation
• Neuroscience and Behaviour research
• Memory, Pain, Epilepsy, Stroke
• Immunopharmacology, Psychopharmacology
Neuroinflammation is currently considered a hallmark of neurodegenerative and neuropsychiatric conditions. Although inflammatory responses mediated by brain immune cells, mainly microglia, are indispensable for tissue homeostasis, overstimulation in the events such as injury and infection may lead to neuronal damage, contributing for the development of neurological morbidities. In this context, accumulating lines of evidence have supported the role of purinergic signalling in neuroinflammation. Upon damage, nucleotides such as ATP, UTP, ADP, UDP, among others, and nucleosides, mainly adenosine, released into the extracellular milieu influence pro- and anti-inflammatory actions. These molecules can bind to their specific purinoceptors, divided into the P1 and P2 families of receptors, expressed on the plasma membrane of cells and mediating a myriad of cellular functions. Nucleotides and nucleosides are eventually degraded by a set of soluble or membrane-bound enzymes, collectively known as ectonucleotidases.
This Research Topic will address some of the main current research on the role of purinergic signaling in neuroinflammation in the events of health and disease conditions. Furthermore, pharmacological targeting of purinergic signaling in distinct scenarios will be a main focus to investigate the landscape of the implications of purinergic system components in the neuroinflammatory responses associated with different pathologies.
Therefore, submission of Original Research, Brief Report, Perspective, Mini-Review, and Review articles focusing on, but not limited to, the following topics are welcome:
• Neuroinflammation, neurodegeneration, neuroregeneration
• Neurodegenerative and neuropsychiatric diseases
• Oxidative/nitrosative stress and neuroinflammation
• Neuroscience and Behaviour research
• Memory, Pain, Epilepsy, Stroke
• Immunopharmacology, Psychopharmacology
