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Several types of brain injuries are causes of acquired temporal lobe epilepsy (TLE). The seizure-free "latent period" that often follows the brain injury is of unknown mechanistic significance but is commonly considered as the "epileptogenic" period characterized by gradual pathogenic processes leading to the onset of clinically detectable epilepsy. Acute convulsive status epilepticus (SE) is often associated with an adverse developmental outcome characterized by learning disabilities related to the cumulative effects of seizures and development of TLE. The symptomatic manifestations of TLE appear only after a widespread irreversible damage of entorhinal cortex, and hippocampus, the brain area most affected by this disease. These pathological features of TLE reduce the possibility of successful therapeutic approaches, often rendering the disease refractory. The difficult clinical management of chronic TLE and the limited success rate of surgical approaches, increase the incapacitating nature of this specific epileptic disorder. Prevention of TLE with an appropriate intervention after a known inciting event (in the case of acquired epilepsy) might represent the most ambitious goal in the clinical treatment of this epileptic disorder, but has been largely unsuccessful to this point. Clinical trials aimed at prevention of chronic epilepsy have often produced negative, disappointing results. However, in most cases, these studies ultimately evaluated the downstream clinical manifestations, failing to monitor early, specific molecular epileptogenic events. Therefore, elucidation of the underlying mechanisms of epileptogenesis, and their time course(s) are essential. The primary purpose of this topic is to collect scientific contributions providing novel insights in the cellular and molecular mechanisms of epileptogenesis as potential targets for innovative therapeutic approaches aimed at preventing the chronic epileptic disorder.

Brain --- Traumatic epilepsy. --- Temporal lobe epilepsy. --- Neuropsychiatry --- Neurosciences --- Wounds and injuries --- Pathophysiology. --- Research. --- Research. --- Epileptogenesis --- TLE prevention --- Epilepsy --- Hippocampal damage --- Neuronal epileptic damage --- Temporal Lobe Epilepsy (TLE)

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

Medicine --- Neurology & clinical neurophysiology --- Status Epilepticus --- Epilepsy --- Seizures --- Anticonvulsants --- Autoimmune epilepsy --- Temporal Lobe Epilepsy --- Epileptogenesis

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Several types of brain injuries are causes of acquired temporal lobe epilepsy (TLE). The seizure-free "latent period" that often follows the brain injury is of unknown mechanistic significance but is commonly considered as the "epileptogenic" period characterized by gradual pathogenic processes leading to the onset of clinically detectable epilepsy. Acute convulsive status epilepticus (SE) is often associated with an adverse developmental outcome characterized by learning disabilities related to the cumulative effects of seizures and development of TLE. The symptomatic manifestations of TLE appear only after a widespread irreversible damage of entorhinal cortex, and hippocampus, the brain area most affected by this disease. These pathological features of TLE reduce the possibility of successful therapeutic approaches, often rendering the disease refractory. The difficult clinical management of chronic TLE and the limited success rate of surgical approaches, increase the incapacitating nature of this specific epileptic disorder. Prevention of TLE with an appropriate intervention after a known inciting event (in the case of acquired epilepsy) might represent the most ambitious goal in the clinical treatment of this epileptic disorder, but has been largely unsuccessful to this point. Clinical trials aimed at prevention of chronic epilepsy have often produced negative, disappointing results. However, in most cases, these studies ultimately evaluated the downstream clinical manifestations, failing to monitor early, specific molecular epileptogenic events. Therefore, elucidation of the underlying mechanisms of epileptogenesis, and their time course(s) are essential. The primary purpose of this topic is to collect scientific contributions providing novel insights in the cellular and molecular mechanisms of epileptogenesis as potential targets for innovative therapeutic approaches aimed at preventing the chronic epileptic disorder.

Brain --- Traumatic epilepsy. --- Temporal lobe epilepsy. --- Neuropsychiatry --- Neurosciences --- Neurology --- Medicine --- Health & Biological Sciences --- Wounds and injuries --- Pathophysiology. --- Research. --- Research. --- Epileptogenesis --- TLE prevention --- Epilepsy --- Hippocampal damage --- Neuronal epileptic damage --- Temporal Lobe Epilepsy (TLE)

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p38 Mitogen activated protein kinases (p38MAPK) are a group of evolutionary conserved protein kinases which are central for cell adaptation to environmental changes as well as for immune response, inflammation, tissue regeneration and tumour formation. The interest in this group of protein kinases has grown continually since their discovery. Recent studies using new genetic and pharmacological tools are providing helpful information on the function of these stress-activated protein kinases and show that they have an acute impact on the development of prevalent diseases related to inflammation, diabetes, neurodegeneration, and cancer. In this Special Issue we present novel advances and review the knowledge on the identification of p38MAPK substrates, functions, and regulation; mechanisms underlying the role of p38MAPK in malignant transformation and other pathologies; and therapeutic opportunities associated with regulation of p38MAPK activity.

arginine methylation --- erythroid differentiation --- MKK3 --- phosphorylation, PRMT1 --- p38 MAPK --- cocaine --- conditioned place preference --- reward --- stress --- anxiety --- depression --- nucleus accumbens --- social interaction --- k opioid receptors --- p38α --- Rab5 --- endosome --- Alzheimer’s --- Lewy Bodies --- amyloid-β --- tau --- α-synuclein --- p38-MAPK α inhibitor --- Alzheimer’s disease --- synaptic plasticity --- neuroinflammation --- β-amyloid --- Tau --- Kv4.2 --- seizure --- temporal lobe epilepsy --- hippocampus --- neuronal firing and excitability --- p38MAPK --- nuclear translocation --- β-like importins --- inflammation --- cancer --- skeletal muscle --- energy metabolism --- signal transduction --- exercise --- type 2 diabetes --- p38 mitogen-activated protein kinase --- bleomycin-induced pulmonary fibrosis --- idiopathic pulmonary fibrosis --- RNA sequencing --- alveolar epithelial type II cells --- MAPK --- p38 --- physiology --- metabolism --- signaling --- hypoxia --- arrhythmia --- MAPK11 --- p38β --- n/a --- Alzheimer's --- Alzheimer's disease

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This collection of articles provides an overview of the current and future methods for applying a personalized medicine approach to the diagnosis, management, and treatment of autism spectrum disorder.

Medicine --- Neurosciences --- fecal metabolites --- ASD --- microbiome --- gastrointestinal symptoms --- Fisher Discriminant Analysis --- digital biomarkers --- wearables --- time series analysis --- autism --- social dyads --- socio-motor parameters --- network connectivity --- non-linear complex dynamics --- stochastic analysis --- autism spectrum disorders --- copy number variants --- females --- Array-Comparative Genomic Hybridization (Array-CGH) --- autism spectrum disorder --- Ehlers-Danlos syndrome --- hypermobility spectrum disorders --- autonomic disorder --- mast cell activation syndrome --- genetic testing --- chromosomal microarray analysis --- whole exome sequencing --- whole genome sequencing --- clinical utility --- polygenic risk scores --- Temple Grandin --- biomarker --- omics --- precision medicine --- proteomics --- transcriptomics --- epigenetics --- metabolomics --- patient stratification --- mitochondria --- oxidative stress --- prenatal environment --- immune dysfunction --- immunoglobulin G --- intravenous immunoglobulin --- energy metabolism --- fatty acid oxidation --- acyl-carnitines --- resveratrol --- integrative --- model --- concomitant --- condition --- disorder --- autism spectrum disorder (ASD) --- genomics --- personalized treatment strategy --- single nucleotide polymorphisms --- clinical decision support tool --- ADHD --- PANDAS --- OCD --- anxiety --- folate receptor alpha --- folates --- pregnancy --- brain development --- fetal development --- cobalamin --- glutathione --- methylation --- methylcobalamin --- redox metabolism --- locked-in network syndrome --- resting-state functional magnetic resonance imaging --- temporal lobe epilepsy --- amygdala --- brain --- COVID-19 --- children --- cytokines --- flavonoids --- inflammation --- luteolin --- mast cells --- microglia --- SARS-CoV-2 --- stress --- nutraceuticals --- survey --- vitamins --- minerals --- B12 --- folinic acid --- quality of life --- parents --- intervention --- systematic review --- medical claims --- logistic regression analysis --- retrospective analysis --- associated risk --- monoamine neurotransmitters --- neurotransmitter deficiency --- cerebral folate deficiency --- folate receptor alpha autoantibodies --- leucovorin --- α-amylase --- cortisol --- heart rate variability --- neuromodulation --- sleep anxiety --- transdermal electrical neuromodulation --- neurostimulation --- fecal metabolites --- ASD --- microbiome --- gastrointestinal symptoms --- Fisher Discriminant Analysis --- digital biomarkers --- wearables --- time series analysis --- autism --- social dyads --- socio-motor parameters --- network connectivity --- non-linear complex dynamics --- stochastic analysis --- autism spectrum disorders --- copy number variants --- females --- Array-Comparative Genomic Hybridization (Array-CGH) --- autism spectrum disorder --- Ehlers-Danlos syndrome --- hypermobility spectrum disorders --- autonomic disorder --- mast cell activation syndrome --- genetic testing --- chromosomal microarray analysis --- whole exome sequencing --- whole genome sequencing --- clinical utility --- polygenic risk scores --- Temple Grandin --- biomarker --- omics --- precision medicine --- proteomics --- transcriptomics --- epigenetics --- metabolomics --- patient stratification --- mitochondria --- oxidative stress --- prenatal environment --- immune dysfunction --- immunoglobulin G --- intravenous immunoglobulin --- energy metabolism --- fatty acid oxidation --- acyl-carnitines --- resveratrol --- integrative --- model --- concomitant --- condition --- disorder --- autism spectrum disorder (ASD) --- genomics --- personalized treatment strategy --- single nucleotide polymorphisms --- clinical decision support tool --- ADHD --- PANDAS --- OCD --- anxiety --- folate receptor alpha --- folates --- pregnancy --- brain development --- fetal development --- cobalamin --- glutathione --- methylation --- methylcobalamin --- redox metabolism --- locked-in network syndrome --- resting-state functional magnetic resonance imaging --- temporal lobe epilepsy --- amygdala --- brain --- COVID-19 --- children --- cytokines --- flavonoids --- inflammation --- luteolin --- mast cells --- microglia --- SARS-CoV-2 --- stress --- nutraceuticals --- survey --- vitamins --- minerals --- B12 --- folinic acid --- quality of life --- parents --- intervention --- systematic review --- medical claims --- logistic regression analysis --- retrospective analysis --- associated risk --- monoamine neurotransmitters --- neurotransmitter deficiency --- cerebral folate deficiency --- folate receptor alpha autoantibodies --- leucovorin --- α-amylase --- cortisol --- heart rate variability --- neuromodulation --- sleep anxiety --- transdermal electrical neuromodulation --- neurostimulation