Neuroprotection: Rescue from Neuronal Death in the Brain
Lee, Bae Hwan
Neuroprotection: Rescue from Neuronal Death in the Brain - Basel, Switzerland MDPI - Multidisciplinary Digital Publishing Institute 2021 - 1 electronic resource (408 p.)
Open Access
Dear Colleagues, The brain is vulnerable to injury. Following injury in the brain, apoptosis or necrosis may occur easily, leading to various functional disabilities. Neuronal death is associated with a number of neurological disorders including hypoxic ischemia, epileptic seizures, and neurodegenerative diseases. The brain subjected to injury is regarded to be responsible for the alterations in neurotransmission processes, resulting in functional changes. Oxidative stress produced by reactive oxygen species has been shown to be related to the death of neurons in traumatic injury, stroke, and neurodegenerative diseases. Therefore, scavenging or decreasing free radicals may be crucial for preventing neural tissues from harmful adversities in the brain. Neurotrophic factors, bioactive compounds, dietary nutrients, or cell engineering may ameliorate the pathological processes related to neuronal death or neurodegeneration and appear beneficial for improving neuroprotection. As a result of neuronal death or neuroprotection, the brain undergoes activity-dependent long-lasting changes in synaptic transmission, which is also known as functional plasticity. Neuroprotection implying the rescue from neuronal death is now becoming one of global health concerns. This Special Issue attempts to explore the recent advances in neuroprotection related to the brain. This Special Issue welcomes original research or review papers demonstrating the mechanisms of neuroprotection against brain injury using in vivo or in vitro models of animals as well as in clinical settings. The issues in a paper should be supported by sufficient data or evidence. Prof. Bae Hwan Lee Guest Editor
Creative Commons
English
books978-3-0365-1995-1 9783036519944 9783036519951
10.3390/books978-3-0365-1995-1 doi
Research & information: general
global cerebral ischemia amiloride sodium–hydrogen exchanger-1 zinc neuronal death neuroprotection neurodegenerative disorder choline acetyltransferase (ChAT) trimethyltin (TMT) bean phosphatidylserine (Bean-PS) brain-derived neurotrophic factor moderate hypoxia physical exercise psychomotor function reaction time cortisol catecholamines nitrite endotheline-1 lactate pyridoxine deficiency ischemia gerbil homocysteine cell death glia neurogenesis N-acetyl-l-cysteine transient receptor potential melastatin 2 neurodegeneration Alzheimer’s disease metabolic disease adiponectin insulin antioxidants stroke preventive gene therapy adenoviral vector VEGF GDNF NCAM human umbilical cord blood mononuclear cells antioxidant brain neurodegenerative disease oxidative stress PGC-1α vascular endothelial growth factor vascular endothelial growth factor receptor 2 PI3K/AKT MEK/ERK status epilepticus hippocampus middle cerebral artery occlusion reperfusion injury lipid emulsion excitotoxicity apoptosis GPR4 receptor MPP+ Parkinson’s disease CRISPR/cas9 ischemic stroke blood brain barrier nanoparticle-based drug delivery brain targeting BDNF miRNAs synaptic plasticity depression glioblastoma astrocytes astrocytic networks connexin 43 calcium activity neural injury nimodipine subarachnoid haemorrhage acid-sensing ion channels oxygen-glucose deprivation liver growth factor inflammation microglia Tg2576 transgenic mice amyloid-beta oculomotor system trophic factors motoneurons axotomy amyotrophic lateral sclerosis electroneutral transport cation-chloride cotransporters KCCs NKCCs WNK-SPAK/OSR1 ascorbic acid aging organotypic hippocampal slice culture n/a
Neuroprotection: Rescue from Neuronal Death in the Brain - Basel, Switzerland MDPI - Multidisciplinary Digital Publishing Institute 2021 - 1 electronic resource (408 p.)
Open Access
Dear Colleagues, The brain is vulnerable to injury. Following injury in the brain, apoptosis or necrosis may occur easily, leading to various functional disabilities. Neuronal death is associated with a number of neurological disorders including hypoxic ischemia, epileptic seizures, and neurodegenerative diseases. The brain subjected to injury is regarded to be responsible for the alterations in neurotransmission processes, resulting in functional changes. Oxidative stress produced by reactive oxygen species has been shown to be related to the death of neurons in traumatic injury, stroke, and neurodegenerative diseases. Therefore, scavenging or decreasing free radicals may be crucial for preventing neural tissues from harmful adversities in the brain. Neurotrophic factors, bioactive compounds, dietary nutrients, or cell engineering may ameliorate the pathological processes related to neuronal death or neurodegeneration and appear beneficial for improving neuroprotection. As a result of neuronal death or neuroprotection, the brain undergoes activity-dependent long-lasting changes in synaptic transmission, which is also known as functional plasticity. Neuroprotection implying the rescue from neuronal death is now becoming one of global health concerns. This Special Issue attempts to explore the recent advances in neuroprotection related to the brain. This Special Issue welcomes original research or review papers demonstrating the mechanisms of neuroprotection against brain injury using in vivo or in vitro models of animals as well as in clinical settings. The issues in a paper should be supported by sufficient data or evidence. Prof. Bae Hwan Lee Guest Editor
Creative Commons
English
books978-3-0365-1995-1 9783036519944 9783036519951
10.3390/books978-3-0365-1995-1 doi
Research & information: general
global cerebral ischemia amiloride sodium–hydrogen exchanger-1 zinc neuronal death neuroprotection neurodegenerative disorder choline acetyltransferase (ChAT) trimethyltin (TMT) bean phosphatidylserine (Bean-PS) brain-derived neurotrophic factor moderate hypoxia physical exercise psychomotor function reaction time cortisol catecholamines nitrite endotheline-1 lactate pyridoxine deficiency ischemia gerbil homocysteine cell death glia neurogenesis N-acetyl-l-cysteine transient receptor potential melastatin 2 neurodegeneration Alzheimer’s disease metabolic disease adiponectin insulin antioxidants stroke preventive gene therapy adenoviral vector VEGF GDNF NCAM human umbilical cord blood mononuclear cells antioxidant brain neurodegenerative disease oxidative stress PGC-1α vascular endothelial growth factor vascular endothelial growth factor receptor 2 PI3K/AKT MEK/ERK status epilepticus hippocampus middle cerebral artery occlusion reperfusion injury lipid emulsion excitotoxicity apoptosis GPR4 receptor MPP+ Parkinson’s disease CRISPR/cas9 ischemic stroke blood brain barrier nanoparticle-based drug delivery brain targeting BDNF miRNAs synaptic plasticity depression glioblastoma astrocytes astrocytic networks connexin 43 calcium activity neural injury nimodipine subarachnoid haemorrhage acid-sensing ion channels oxygen-glucose deprivation liver growth factor inflammation microglia Tg2576 transgenic mice amyloid-beta oculomotor system trophic factors motoneurons axotomy amyotrophic lateral sclerosis electroneutral transport cation-chloride cotransporters KCCs NKCCs WNK-SPAK/OSR1 ascorbic acid aging organotypic hippocampal slice culture n/a