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The Reeler mutation was so named because of the alterations in gait that characterize homozygous mice. Several decades after the description of the Reeler phenotype, the mutated protein was discovered and named Reelin (Reln). Reln controls a number of fundamental steps in embryonic and postnatal brain development. A prominent embryonic function is the control of radial neuronal migration. As a consequence, homozygous Reeler mutants show disrupted cell layering in cortical brain structures. Reln also promotes postnatal neuronal maturation. Heterozygous mutants exhibit defects in dendrite extension and synapse formation, correlating with behavioral and cognitive deficits that are detectable at adult ages. The Reln-encoding gene is highly conserved between mice and humans. In humans, homozygous RELN mutations cause lissencephaly with cerebellar hypoplasia, a severe neuronal migration disorder that is reminiscent of the Reeler phenotype. In addition, RELN deficiency or dysfunction is also correlated with psychiatric and cognitive disorders, such as schizophrenia, bipolar disorder and autism, as well as some forms of epilepsy and Alzheimer's disease. Despite the wealth of anatomical studies of the Reeler mouse brain, and the molecular dissection of Reln signaling mechanisms, the consequences of Reln deficiency on the development and function of the human brain are not yet completely understood. This Research Topic include reviews that summarize our current knowledge of the molecular aspects of Reln function, original articles that advance our understanding of its expression and function in different brain regions, and reviews that critically assess the potential role of Reln in human psychiatric and cognitive disorders.

Neurons --- neuronal migration --- Schizophrenia --- Depression --- Neuronal Death --- Reeler --- Synapses --- autism --- intracellular pathways

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The present studies evaluated the effect of chronic intraventricular microinfusion of norepinephrine (NE) to examine if higher levels of intracerebral NE could protect against the development of delayed neuronal death (DND) in the hippocampus of a transient forebrain ischaemia model. Small cannulas connected to osmotic minipumps were stereotactically placed in the lateral ventricle, and NE (40 mu M) was pumped at the rate of 0.5 mu l/hour for periods of up to 14 days. Brain tissue was then analysed for the total NE content at 2.5 mm intervals from the cannula tip, using high pressure liquid chromatography, The result of these preliminary studies showed a 5 to 40-fold increase in the NE levels in the specimens on the infusion side and a 2 to 3-fold increase on the non-infusion side. The number of surviving pyramidal neurones in the hippocampal CA1 region were then compared between the ipsilateral and contralateral hemispheres of the brains obtained from experimental and control animals. Significant suppression of neuronal death was demonstrated in the presence of increased levels of exogenous NE on the infusion side. These studies suggest that intraventricular administration of NE is feasible and that the resulting higher levels of NE may attenuate the phenomenon of DND in the hippocampus, possibly by a direct protective action upon the neurones

Animal. --- Animals. --- Brain. --- Ca1. --- Cannula. --- Control. --- Damage. --- Death. --- Delayed neuronal death. --- Density. --- Development. --- Forebrain ischemia. --- Gerbil hippocampus. --- Hemisphere. --- Hippocampal. --- Hippocampus. --- Increase. --- Injury. --- Ischaemia. --- Ischemic brain. --- Level. --- Locus coeruleus. --- Model. --- Neuronal death. --- Neuronal. --- Norepinephrine. --- Periods. --- Production. --- Rat. --- Suppression. --- Time. --- Transient ischemia.

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Five min bilateral carotid artery occlusion (BCO) in gerbils results in selective degeneration of neurons in the hippocampus, striatum and cortex, and an increase in spontaneous locomotor activity. These phenomena were examined to determine if an association could be made between the site or degree of neuronal degeneration and the increase in locomotor activity. The distance traveled by the BCO gerbils in a novel cage 1, 4, and 28 days after a 5 min occlusion was significantly greater than control. The extensive pyramidal cell damage in the CA1 region of the hippocampus in BCO gerbils was associated with the significant increase in locomotor activity. The increase in locomotor activity did not correlate with either the striatal or cortical damage present. The increase in gerbil locomotor activity following a 5 min BCO can be used as a predictor of CA1 damage, but not as a predictor of striatal or cortical damage

Activity. --- Artery occlusion. --- Aspartate. --- Association. --- Ca1. --- Cage. --- Cerebral ischemia. --- Cerebral-ischemia. --- Control. --- Cortex. --- Damage. --- Death. --- Degeneration. --- Delayed neuronal death. --- Distance. --- Forebrain ischemia. --- Gerbil. --- Gerbils. --- Hippocampus. --- Increase. --- Intracerebral microdialysis. --- Ireland. --- Ischemia. --- Locomotor activity. --- Locomotor-activity. --- Model. --- Mongolian gerbils. --- Neuronal damage. --- Neuronal degeneration. --- Neuronal. --- Neurons. --- Selective vulnerability. --- Striatum. --- Time. --- Transient forebrain ischemia.

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The Mediterranean diet is a model of eating based on the traditional foods and drinks of the countries surrounding the Mediterranean Sea. The cultural and the nutritional aspects of the multisecular Mediterranean civilization include diet as a central element of health and wellbeing, including wine, if it is consumed in moderation. In recent decades, it has been promoted worldwide (UNESCO 2010) as one of the healthiest dietary patterns. The objective of this book is to bring the role of wine as part of the Mediterranean diet to light, especially through policy makers, the medical world, and vectors of images.

Humanities --- Social interaction --- apigenin --- docosahexaenoic acid --- eicosapentaenoic acid --- 7-ketocholesterol --- α-linolenic acid --- Mediterranean diet --- N2a cells --- oleic acid --- oxidative stress --- quercetin --- resveratrol. --- wine --- ethanol --- acetaldehyde --- oral cavity cancer --- carcinogenesis --- resveratrol --- polydatin --- peonidin 3-O-glucoside --- malvidin 3-O-glucoside --- quercetin 3-O-glucoside --- (+)-catechin --- (+)-taxifolin --- apoptosis --- neuronal death --- cerebellum --- polyphenols --- flavonoids --- diet --- clinical trials --- metabolites --- resveratrol butyrate ester --- butyric acid --- Steglich esterification --- prevent fat accumulation --- wine intake --- cardiovascular disease --- cancer --- dementia --- red wine extract --- AMD --- retinal cells --- ARPE-19 --- degenerative diseases --- ocular diseases --- olive oil --- alcohol --- phytochemicals --- tyrosol --- inflammatory bowel disease --- Crohn’s disease --- ulcerative colitis --- inflammation --- neurodegeneration --- neuroprotection --- therapeutic targets --- pharmacology --- novel delivery system --- postovulatory aging --- oocyte quality --- reactive oxygen species --- n/a --- Crohn's disease

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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

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 --- sodium-hydrogen exchanger-1 --- Alzheimer's disease --- Parkinson's disease