Neuroinflammation is one of the host defensive mechanisms through which the nervous system protects itself from many assaults. The neuroinflammatory response aims to protect neuronal integrity by removing the noxa or damaged tissue, repairing the neural tissue, thus restoring neuronal homeostasis. However, depending on the type of injury, its duration and intensity, the neuroinflammation process can lead to oxidative stress, with the increased release of pro-inflammatory cytokines which may trigger a series of pathological cascades which will directly or indirectly cause cell death, disruption of the blood–brain barrier, cerebral edema, and tissue hemorrhage. In the latter case, inflammation may be a negative contributing factor against acute and chronic nervous system disorders.
Neuroinflammation may be triggered by a wide spectrum of inner and external insults, ranging from infectious agents, ischemic and hemorrhagic accidents, traumatic brain or spinal cord injuries, depression, migraine, epilepsy, to complex neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease or even epigenetic-based disorders. Recently, it has become increasingly evident that the digestive microbiome may influence neuroinflammatory-based diseases by a humoral pathway carrying microbe’s metabolites or its metabolic derived byproducts, or even by the bidirectional autonomic pathway between the gut and the central nervous system. All these events lead to blood-brain barrier breakdown, neuronal injury, oxidative stress, increased matrix metalloproteinase production, microglial activation, and infiltration of peripheral immune cells into the neural tissue. At the molecular level, the transcription factor NF-?B, for instance, seems to play a crucial role in the initiation and regulation of several inflammatory processes attributed to a plethora of neurodegenerative diseases. In order to understand how the aforementioned disorders occur, new research should shed more light on these problems, as well as discover new treatments to alleviate or neutralize these neuroinflammatory-based disorders.
The proposed research topic aims to unravel the most relevant neuroinflammatory aspects in the context of a wide variety of central or peripheral neural damage. For this, it is necessary to elucidate its mechanism of action and/or propose innovative therapeutic targets, viewed from a molecular perspective towards an integrative profile. Original research articles, reviews, short communications, and clinical reports are welcome. Molecular and cellular biology, biochemical, biophysical, neuroanatomical, imaging, and pharmacological studies are within the scope of this research topic.
Specific topics addressed here (but not limited to) in neuroinflammatory pathologies may include:
• Neurodegenerative diseases
• Traumatic brain injury
• Neuroinfectious diseases
• Neuroepigenetic-based disorders
• Neuro-oncology
• Microbiota-gut-brain axis imbalance
• Stress-related illnesses
Neuroinflammation is one of the host defensive mechanisms through which the nervous system protects itself from many assaults. The neuroinflammatory response aims to protect neuronal integrity by removing the noxa or damaged tissue, repairing the neural tissue, thus restoring neuronal homeostasis. However, depending on the type of injury, its duration and intensity, the neuroinflammation process can lead to oxidative stress, with the increased release of pro-inflammatory cytokines which may trigger a series of pathological cascades which will directly or indirectly cause cell death, disruption of the blood–brain barrier, cerebral edema, and tissue hemorrhage. In the latter case, inflammation may be a negative contributing factor against acute and chronic nervous system disorders.
Neuroinflammation may be triggered by a wide spectrum of inner and external insults, ranging from infectious agents, ischemic and hemorrhagic accidents, traumatic brain or spinal cord injuries, depression, migraine, epilepsy, to complex neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease or even epigenetic-based disorders. Recently, it has become increasingly evident that the digestive microbiome may influence neuroinflammatory-based diseases by a humoral pathway carrying microbe’s metabolites or its metabolic derived byproducts, or even by the bidirectional autonomic pathway between the gut and the central nervous system. All these events lead to blood-brain barrier breakdown, neuronal injury, oxidative stress, increased matrix metalloproteinase production, microglial activation, and infiltration of peripheral immune cells into the neural tissue. At the molecular level, the transcription factor NF-?B, for instance, seems to play a crucial role in the initiation and regulation of several inflammatory processes attributed to a plethora of neurodegenerative diseases. In order to understand how the aforementioned disorders occur, new research should shed more light on these problems, as well as discover new treatments to alleviate or neutralize these neuroinflammatory-based disorders.
The proposed research topic aims to unravel the most relevant neuroinflammatory aspects in the context of a wide variety of central or peripheral neural damage. For this, it is necessary to elucidate its mechanism of action and/or propose innovative therapeutic targets, viewed from a molecular perspective towards an integrative profile. Original research articles, reviews, short communications, and clinical reports are welcome. Molecular and cellular biology, biochemical, biophysical, neuroanatomical, imaging, and pharmacological studies are within the scope of this research topic.
Specific topics addressed here (but not limited to) in neuroinflammatory pathologies may include:
• Neurodegenerative diseases
• Traumatic brain injury
• Neuroinfectious diseases
• Neuroepigenetic-based disorders
• Neuro-oncology
• Microbiota-gut-brain axis imbalance
• Stress-related illnesses