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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

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• Reference Manager
• EndNote
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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

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The book highlights important aspects of Molecular Psychiatry, including molecular mechanisms, animal models, biomarkers, advanced methods, drugs and antidepressant response, as well as genetics and epigenetics. Molecular mechanisms are a vital part of the search for the biological basis of psychiatric disorders, providing molecular hints that can later be tested as biomarkers or targets for drug development. Animal models represent a commonly used approach to aid in this bench-to-bed translation; the examples here are social defeat stress and the Roman High-Avoidance (RHA) and the Roman Low-Avoidance (RLA) rats. For biomarkers, psychiatric disorders pose a particular challenge due to the tissue specificity of many currently investigated biomarkers; i.e., not all blood-based measures directly represent changes in the brain. The Ebook includes five articles focused on the challenges of identifying clinically and biologically relevant biomarkers for psychiatric disorders. Scientific progress typically is fostered by the development of new methods. The application of machine learning methods for the proper analysis of Big Data and induced pluripotent stem cells are examples outlined in this Ebook. Furthermore, three articles are devoted to the understanding of the mechanisms of actions of existing drugs with the ultimate goal of identifying ways to predict treatment response in patients. Finally, three articles deepen the insight into the genetics and epigenetics of psychiatric disorders.

Medicine --- Mental health services --- cardiovascular disease --- cell adhesion molecules --- immunology --- inflammation --- nervous system --- schizophrenia --- bipolar disorder --- major depressive disorder --- DNA methylation --- response variability --- antipsychotics --- drug design --- multi-target drugs --- polypharmacology --- multi-task learning --- machine learning --- biomarker discovery --- psychiatry --- serotonin --- 5-HT 4 receptor --- 5-HT4R --- depression --- mood disorder --- expression --- Alzheimer's disease --- cognition --- Parkinson's disease --- forced swimming --- Roman rat lines --- stress --- hippocampus --- BDNF --- trkB --- PSA-NCAM --- western blot --- immunohistochemistry --- general cognitive function --- intelligence --- GWAS --- genetic correlation --- childhood-onset schizophrenia (COS) --- induced pluripotent stem cell (iPSC) --- copy number variation (CNV) --- early neurodevelopment --- neuronal differentiation --- synapse --- dendritic arborization --- miRNAs --- stress physiology --- cytoskeleton --- actin dynamics --- DRR1 --- TU3A --- FAM107A --- acid sphingomyelinase --- alcohol dependence --- liver enzymes --- sphingolipid metabolism --- withdrawal --- Hsp90 --- GR --- stress response --- steroid hormones --- molecular chaperones --- psychiatric disease --- circadian rhythms --- FKBP51 --- FKBP52 --- CyP40 --- PP5 --- DISC1 --- neurodevelopment --- CRMP-2 --- proteomics --- antidepressant treatment --- HPA axis --- gene expression --- FKBP5 --- sleep --- sleep EEG --- biomarkers --- antidepressants --- cordance --- gender --- sex difference --- antidepressant --- rapid-acting --- Ketamine --- endocrinology --- (2R,6R)-Hydroxynorketamine --- electroconvulsive therapy --- basic-helix-loop-helix --- brain --- coactivator --- glucocorticoids --- mineralocorticoid receptor knockout --- transcription biology --- dopaminergic gene polymorphisms --- affective temperament --- obesity --- alpha-synuclein --- SNCA --- major depression --- Hamilton Scale of Depression --- chemokines --- neuroinflammation --- social defeat --- Immune response --- T cells --- susceptibility --- resilience --- Treg cells --- Th17 cells --- behavior --- PPARγ