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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

Science: general issues --- Neurosciences --- neurodegeneration --- neuroprotection --- Alzheimer’s disease --- ischemic tolerance --- hypoxic preconditioning --- mitochondria --- fatty acids --- miRNAs --- nanoparticles --- prenatal hypoxia --- hypothermia --- heat acclimation --- homocysteine

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Cerebral ischemia is one of the most common causes of dementia, which develops in more than half of patients after an ischemic episode. The main mechanism is thought to be pathological changes in the hippocampus, especially in the CA1 area, underlying episodic memory impairment, which is the earliest and most important clinical symptom of post-ischemic dementia. The 13 chapters of this book present a new picture of ischemic brain disease, synthesizing the latest data on disease mechanisms, care for patients with this disease, and potential therapeutic targets. The authors present the characteristics of cerebral ischemia from pregnancy and childhood through adolescence to adulthood. The first two chapters provide a snapshot of the anatomy of the cerebral cortex and the hippocampus, the most affected brain structures after cerebral ischemia. This is followed by nine chapters that present a comprehensive view of the pathological mechanisms of cerebral ischemia, and how a deep understanding of these pathomechanisms hold the key for the discovery and development of novel therapies to help patients affected by cerebral ischemia. Chapter 12 shares real-life experience and challenges of rehabilitating patients into the community after cerebral ischemia, and chapter 13 analyzes the social risk variations, including gender inequality, in the reintegration of post-ischemic stroke patients. Although primarily aimed at scientists and clinicians, the contents of the book will be of interest to all those who are interested in cerebral ischemia, including patients and their caregivers.

MJN --- Anatomy of the Cerebral Cortex; Anatomy of the Hippocampus; Genes Associated with Alzheimer’s Disease; Hypoxic-Ischemic Brain Injury; Perinatal Asphyxia; Ischemic Brain Injury; Hyperhomocysteinemia; Exosomes in Post-Ischemic Brain; Neuroinflammation in Post-Ischemic Brain; Neurovascular Reactivity in Cerebral Ischemia; Cathepsin B in Ischemia-Reperfusion Injury After Stroke; Curcumin in Post-Ischemic Brain; Treating Cerebral Ischemia; Experimental Stroke Research; Community-Based Rehabilitation in Japan; Social Risk Variation Across Reintegration of Post-Ischemic Stroke Patients

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Cerebral ischemia is one of the most common causes of dementia, which develops in more than half of patients after an ischemic episode. The main mechanism is thought to be pathological changes in the hippocampus, especially in the CA1 area, underlying episodic memory impairment, which is the earliest and most important clinical symptom of post-ischemic dementia. The 13 chapters of this book present a new picture of ischemic brain disease, synthesizing the latest data on disease mechanisms, care for patients with this disease, and potential therapeutic targets. The authors present the characteristics of cerebral ischemia from pregnancy and childhood through adolescence to adulthood. The first two chapters provide a snapshot of the anatomy of the cerebral cortex and the hippocampus, the most affected brain structures after cerebral ischemia. This is followed by nine chapters that present a comprehensive view of the pathological mechanisms of cerebral ischemia, and how a deep understanding of these pathomechanisms hold the key for the discovery and development of novel therapies to help patients affected by cerebral ischemia. Chapter 12 shares real-life experience and challenges of rehabilitating patients into the community after cerebral ischemia, and chapter 13 analyzes the social risk variations, including gender inequality, in the reintegration of post-ischemic stroke patients. Although primarily aimed at scientists and clinicians, the contents of the book will be of interest to all those who are interested in cerebral ischemia, including patients and their caregivers.

MJN --- Anatomy of the Cerebral Cortex; Anatomy of the Hippocampus; Genes Associated with Alzheimer’s Disease; Hypoxic-Ischemic Brain Injury; Perinatal Asphyxia; Ischemic Brain Injury; Hyperhomocysteinemia; Exosomes in Post-Ischemic Brain; Neuroinflammation in Post-Ischemic Brain; Neurovascular Reactivity in Cerebral Ischemia; Cathepsin B in Ischemia-Reperfusion Injury After Stroke; Curcumin in Post-Ischemic Brain; Treating Cerebral Ischemia; Experimental Stroke Research; Community-Based Rehabilitation in Japan; Social Risk Variation Across Reintegration of Post-Ischemic Stroke Patients

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Studies focusing on the perinatal period face unique challenges, yet research in this area is extremely important, as this period of life is highly delicate and adverse events might have a long-lasting impact. With the advent of powerful high-resolution and high-throughput analytical methods, researchers have started to successfully develop and implement novel approaches in this area. New insights have great potential to be translated into novel diagnostic tools, as well as alternative preventive and treatment approaches. This book collects a series of timely review and original research articles focusing on metabolomic, oxidative, and nitrosative stress in the perinatal period.We would like to thank all involved authors for their high-quality contributions and their commitment to the publication of this work and hope that this book will be a useful resource for students, scientists, and doctors working in this specific area of application.

glutathione --- glutamate --- oxidative stress --- hypoxia ischemia --- endotoxin --- magnetic resonance spectroscopy --- N-acetylcysteine --- vitamin D --- neonatal HIE --- MRS --- preterm birth --- sex differences --- male disadvantage --- female advantage --- bronchopulmonary dysplasia --- retinopathy of prematurity --- necrotizing enterocolitis --- intraventricular hemorrhage --- periventricular leukomalacia --- mortality --- transposition of the great arteries --- balloon atrial septostomy --- hypoxemia --- metabolomics --- newborn --- liquid chromatography-mass spectrometry (LC-MS) --- allopurinol --- hypothermia --- hypoxic-ischemic encephalopathy --- oxidative damage --- donor milk --- treatment --- Holder pasteurization --- breastmilk --- preterm --- antioxidant capacity --- asphyxia neonatorum --- non-invasive diagnostics --- saliva --- neonatal hypoxia–ischemia --- kynurenic acid (KYNA) --- neuroprotection --- hyperoxia --- prematurity --- n/a --- neonatal hypoxia-ischemia

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The sense of hearing is vulnerable to environmental challenges, such as exposure to noise. More than 1.5 billion people experience some decline in hearing ability during their lifetime, of whom at least 430 million will be affected by disabling hearing loss. If not identified and addressed in a timely way, hearing loss can severely reduce the quality of life at various stages. Some causes of hearing loss can be prevented, for example from occupational or leisure noise. The World Health Organization estimates that more than 1 billion young people put themselves at risk of permanent hearing loss by listening to loud music over long periods of time. Mitigating such risks through public health action is essential to reduce the impact of hearing loss in the community. The etiology of sensorineural hearing loss is complex and multifactorial, arising from congenital and acquired causes. This book highlights the diverse range of approaches to sensorineural hearing loss, from designing new animal models of age-related hearing loss, to the use of microRNAs as biomarkers of cochlear injury and drug repurposing for the therapy of age-related and noise-induced hearing loss. Further investigation into the underlying molecular mechanisms of sensorineural hearing loss and the integration of the novel drug, cell, and gene therapy strategies into controlled clinical studies will permit significant advances in a field where there are currently many unmet needs.

Medicine --- brain-derived neurotrophic factor --- TrkB --- inner ear --- development --- zebrafish --- mitochondria dysfunction --- reactive oxygen species --- hypoxic --- d-galactose --- high-fat diet --- aging --- hearing loss --- astrocytes --- auditory brainstem --- lateral superior olive --- gap junctions --- voltage-activated calcium channel 1.3 --- otoferlin --- spontaneous activity --- deafness --- circadian dysregulation --- clock genes --- noise-induced hearing loss --- sensory hair cells --- synaptic ribbons --- sensorineural hearing loss --- hyperbaric oxygenation --- adjunctive therapy --- microRNAs --- cochlear nucleus --- inferior colliculus --- neuroplasticity --- noise-induced cochlear injury --- cochlear rescue --- otoprotection --- adenosine A1 receptor --- regulator of G protein signalling 4 --- CCG-4986 --- intratympanic drug delivery --- potassium voltage-gated channel subfamily q member 4 --- potassium --- nonsyndromic hearing loss --- KCNQ4 activator --- age-related hearing loss --- selegiline --- chronic oral treatment --- hearing protection --- mouse model --- n/a