TY  - GEN
AU  - Lee,Bae Hwan
AU  - Lee,Bae Hwan
TI  - Neuroprotection: Rescue from Neuronal Death in the Brain
SN  - books978-3-0365-1995-1
PY  - 2021///
CY  - Basel, Switzerland
PB  - MDPI - Multidisciplinary Digital Publishing Institute
KW  - Research & information: general
KW  - bicssc
KW  - global cerebral ischemia
KW  - amiloride
KW  - sodium-hydrogen exchanger-1
KW  - zinc
KW  - neuronal death
KW  - neuroprotection
KW  - neurodegenerative disorder
KW  - choline acetyltransferase (ChAT)
KW  - trimethyltin (TMT)
KW  - bean phosphatidylserine (Bean-PS)
KW  - brain-derived neurotrophic factor
KW  - moderate hypoxia
KW  - physical exercise
KW  - psychomotor function
KW  - reaction time
KW  - cortisol
KW  - catecholamines
KW  - nitrite
KW  - endotheline-1
KW  - lactate
KW  - pyridoxine deficiency
KW  - ischemia
KW  - gerbil
KW  - homocysteine
KW  - cell death
KW  - glia
KW  - neurogenesis
KW  - N-acetyl-l-cysteine
KW  - transient receptor potential melastatin 2
KW  - neurodegeneration
KW  - Alzheimer's disease
KW  - metabolic disease
KW  - adiponectin
KW  - insulin
KW  - antioxidants
KW  - stroke
KW  - preventive gene therapy
KW  - adenoviral vector
KW  - VEGF
KW  - GDNF
KW  - NCAM
KW  - human umbilical cord blood mononuclear cells
KW  - antioxidant
KW  - brain
KW  - neurodegenerative disease
KW  - oxidative stress
KW  - PGC-1α
KW  - vascular endothelial growth factor
KW  - vascular endothelial growth factor receptor 2
KW  - PI3K/AKT
KW  - MEK/ERK
KW  - status epilepticus
KW  - hippocampus
KW  - middle cerebral artery occlusion
KW  - reperfusion injury
KW  - lipid emulsion
KW  - excitotoxicity
KW  - apoptosis
KW  - GPR4 receptor
KW  - MPP+
KW  - Parkinson's disease
KW  - CRISPR/cas9
KW  - ischemic stroke
KW  - blood brain barrier
KW  - nanoparticle-based drug delivery
KW  - brain targeting
KW  - BDNF
KW  - miRNAs
KW  - synaptic plasticity
KW  - depression
KW  - glioblastoma
KW  - astrocytes
KW  - astrocytic networks
KW  - connexin 43
KW  - calcium activity
KW  - neural injury
KW  - nimodipine
KW  - subarachnoid haemorrhage
KW  - acid-sensing ion channels
KW  - oxygen-glucose deprivation
KW  - liver growth factor
KW  - inflammation
KW  - microglia
KW  - Tg2576 transgenic mice
KW  - amyloid-beta
KW  - oculomotor system
KW  - trophic factors
KW  - motoneurons
KW  - axotomy
KW  - amyotrophic lateral sclerosis
KW  - electroneutral transport
KW  - cation-chloride cotransporters
KW  - KCCs
KW  - NKCCs
KW  - WNK-SPAK/OSR1
KW  - ascorbic acid
KW  - aging
KW  - organotypic hippocampal slice culture
KW  - n/a
N1  - Open Access
N2  - 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
UR  - https://mdpi.com/books/pdfview/book/4368
UR  - https://directory.doabooks.org/handle/20.500.12854/76898
ER  -