Neuroprotection: Rescue from Neuronal Death in the Brain

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 neurodegener...

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description 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
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spelling doab-20.500.12854ir-768982024-03-27T16:34:28Z Neuroprotection: Rescue from Neuronal Death in the Brain Lee, Bae Hwan 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 thema EDItEUR::G Reference, Information and Interdisciplinary subjects::GP Research and information: general 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 2022-01-11T13:45:35Z 2022-01-11T13:45:35Z 2021 book ONIX_20220111_9783036519944_633 9783036519944 9783036519951 https://directory.doabooks.org/handle/20.500.12854/76898 eng image/jpeg Attribution 4.0 International https://mdpi.com/books/pdfview/book/4368 https://mdpi.com/books/pdfview/book/4368 MDPI - Multidisciplinary Digital Publishing Institute 10.3390/books978-3-0365-1995-1 10.3390/books978-3-0365-1995-1 46cabcaa-dd94-4bfe-87b4-55023c1b36d0 9783036519944 9783036519951 408 Basel, Switzerland open access
spellingShingle 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
thema EDItEUR::G Reference, Information and Interdisciplinary subjects::GP Research and information: general
Neuroprotection: Rescue from Neuronal Death in the Brain
title Neuroprotection: Rescue from Neuronal Death in the Brain
title_full Neuroprotection: Rescue from Neuronal Death in the Brain
title_fullStr Neuroprotection: Rescue from Neuronal Death in the Brain
title_full_unstemmed Neuroprotection: Rescue from Neuronal Death in the Brain
title_short Neuroprotection: Rescue from Neuronal Death in the Brain
title_sort neuroprotection rescue from neuronal death in the brain
topic 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
thema EDItEUR::G Reference, Information and Interdisciplinary subjects::GP Research and information: general
topic_facet 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
thema EDItEUR::G Reference, Information and Interdisciplinary subjects::GP Research and information: general
url ONIX_20220111_9783036519944_633