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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 --- Endocrinology --- cancer --- circadian rhythm --- clock genes --- metabolism --- neurological diseases --- shift work --- cancer --- circadian rhythm --- clock genes --- metabolism --- neurological diseases --- shift work

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The mammalian body is a wonder of complexity, preparing itself to thrive, accordingly to predictable changes in its environment, through bidirectional interactions between the circadian clock system and metabolic regulation pathways. 
This circadian system is composed of several clocks: a master clock in the suprachiasmatic nucleus in the hypothalamus, synchronising the entire body with light/dark cycles; autonomous molecular oscillators inside most of the cells including loops of transcription and translation of core clock genes and post-translational modifications through reduction/oxidation cycles; feedforward/feedback control over important hormonal axes such as the entero-insular axis or the hypothalamic-pituitary-adrenal (HPA) axis. This interlocking activity is particularly at state within metabolic syndromes, be that in mice as well as in human or horses. 
The aim of our work is to underline the importance of genetic factors intertwined with environmental factors such as time of food intake, composition of diet, exercise rate, in the pathology of this comparable diseases, by linking the many examples of circadian clock system disruptions with the resulting metabolic issues. L’organisme mammifère est, de par sa complexité exemplaire, préparé à survivre le mieux possible en cohérence avec les changements quotidiens intervenant dans son environnement. Ceci est permis notamment par les interactions bidirectionnelles entre le système circadien et les voies de régulation métaboliques. Le système circadien est composé de plusieurs « horloges » : un chef d’orchestre dans le noyau suprachiasmatique situé dans l’hypothalamus relie les cycles de nuit et jour au reste du corps ; des oscillateurs autonomes au sein de la plupart des cellules de l’organisme, comprenant des boucles de transcription/traduction des gènes constituant le cœur de l’horloge et des modifications posttraductionnelles à travers des cycles de réduction/oxydation ; des effets de contrôle/rétro-contrôle sur des axes hormonaux importants tels que l’axe hypotalamo-hypophyso-surrénalien ou entéroinsulinaire. Ces activités intrinsèquement liées sont particulièrement illustrées par les syndromes métaboliques explicités chez la souris, l’humain et les équidés. Le but de ce travail est de mettre en évidence l’importance des facteurs génétiques, en dialogue constant avec des facteurs environnementaux tels que les horaires de repas et la composition du régime alimentaire et sportif, par le biais de nombreux exemples de ruptures du système circadien et des conséquences métaboliques qui en découlent.

clock genes --- hormonal cycles --- equine metabolic syndrome --- genetic predispositions --- melatonin --- Sciences du vivant > Génétique & processus génétiques --- Sciences du vivant > Médecine vétérinaire & santé animale

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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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Alzheimer’s disease (AD) represents the most common form of dementia in the elderly population worldwide. AD is characterized by progressive neurodegeneration that leads to a gradual deterioration of memory and other cognitive functions. Given the global prevalence and impact of AD, there is a critical need to establish biomarkers that can be used to detect AD in individuals before the onset of clinical signs and provide mitigating therapeutics. The aim of this Special Issue is to discuss the current knowledge as well as future perspectives on the role of biomarkers in the screening, diagnosis, treatment and follow-up of AD.

Medicine --- flotillin --- Alzheimer's disease --- biomarker --- exosomes --- beta-amyloid --- Tau --- aging --- biomarkers --- cytokines --- cognitive decline --- metabolomics --- neuroinflammation --- multivariate analysis --- physical performance --- person-tailored --- PET/CT --- (18F)FDG --- neuropsychological assessment --- APP mutations --- APOE alleles --- PSEN1 --- PSEN2 --- germline mutations --- late onset AD --- early onset AD --- familial AD --- genetics of AD --- mitochondrial spare respiratory capacity --- mitochondrial --- membrane potential --- glycolytic reserve --- semantic memory --- phonemic fluency --- episodic memory --- neuropsychology --- neuroimaging --- Alzheimer's disease --- mild cognitive impairment --- EEG --- TMS --- obesity --- diabetes --- inflammation --- Amyloid Beta --- mitochondrial dysfunction --- nutrition --- omega-3 fatty acids --- antioxidant --- carotenoids --- vitamin E --- cognition --- older adults --- ageing --- subjective cognitive decline --- clock genes --- Clock --- ApoE --- cardiovascular risk factors --- Alzheimer disease --- semantic priming --- amyloid beta --- cerebrospinal fluid --- amyloid beta peptide --- total tau --- phosphorylated tau --- diagnosis --- drug development --- clinical trials --- diagnostic research --- virus --- bacteria --- dementia --- blood --- behavioral and psychological symptoms of dementia (BPSD) --- Alzheimer's disease (AD) --- neuropsychiatry inventory scale (NPI) --- endophenotypes --- CART analysis --- MTHFR --- APOE --- COMT --- genetic variants --- early diagnosis --- biofluids --- amyloid cascade hypothesis --- glucose metabolism --- adipose tissue dysfunction --- energetic metabolism --- lysosomes dysfunction --- Type-3-Diabetes --- neurodegeneration --- amyloid --- tau --- soluble TREM2 --- NfL --- Multiplex --- SiMoA --- diagnostics --- messenger RNA --- microRNA --- neurotropic microbes --- precision medicine --- prognostics --- synaptic biomarkers --- neurofilament light chain --- flotillin --- Alzheimer's disease --- biomarker --- exosomes --- beta-amyloid --- Tau --- aging --- biomarkers --- cytokines --- cognitive decline --- metabolomics --- neuroinflammation --- multivariate analysis --- physical performance --- person-tailored --- PET/CT --- (18F)FDG --- neuropsychological assessment --- APP mutations --- APOE alleles --- PSEN1 --- PSEN2 --- germline mutations --- late onset AD --- early onset AD --- familial AD --- genetics of AD --- mitochondrial spare respiratory capacity --- mitochondrial --- membrane potential --- glycolytic reserve --- semantic memory --- phonemic fluency --- episodic memory --- neuropsychology --- neuroimaging --- Alzheimer's disease --- mild cognitive impairment --- EEG --- TMS --- obesity --- diabetes --- inflammation --- Amyloid Beta --- mitochondrial dysfunction --- nutrition --- omega-3 fatty acids --- antioxidant --- carotenoids --- vitamin E --- cognition --- older adults --- ageing --- subjective cognitive decline --- clock genes --- Clock --- ApoE --- cardiovascular risk factors --- Alzheimer disease --- semantic priming --- amyloid beta --- cerebrospinal fluid --- amyloid beta peptide --- total tau --- phosphorylated tau --- diagnosis --- drug development --- clinical trials --- diagnostic research --- virus --- bacteria --- dementia --- blood --- behavioral and psychological symptoms of dementia (BPSD) --- Alzheimer's disease (AD) --- neuropsychiatry inventory scale (NPI) --- endophenotypes --- CART analysis --- MTHFR --- APOE --- COMT --- genetic variants --- early diagnosis --- biofluids --- amyloid cascade hypothesis --- glucose metabolism --- adipose tissue dysfunction --- energetic metabolism --- lysosomes dysfunction --- Type-3-Diabetes --- neurodegeneration --- amyloid --- tau --- soluble TREM2 --- NfL --- Multiplex --- SiMoA --- diagnostics --- messenger RNA --- microRNA --- neurotropic microbes --- precision medicine --- prognostics --- synaptic biomarkers --- neurofilament light chain