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Down syndrome (DS), caused by the triplication of chromosome 21, is the most common genetic cause of intellectual disability (ID). Individuals with DS commonly exhibit unique neuropsychological profiles that emerge during specific developmental stages across the lifespan, often characterized by early developmental delay, cognitive strengths and weaknesses, behavior and mental health issues, and age-related cognitive decline, frequently resulting in early-onset Alzheimer’s disease. These profiles are unique compared to other individuals with ID and reflect the genetic mechanisms and neuroanatomic features underlying the distinct neuropsychological phenotype associated with DS. This Special Issue aims to highlight the recent advancements in understanding the neuropsychological phenotype associated with DS across the lifespan. The lifespan perspective will cover four developmental stages: (1) early childhood; (2) school age; (3) young adulthood, and (4) older adulthood. Authors contributed cutting-edge original research studies and comprehensive reviews that address a broad range of topics related to DS, including early developmental trajectories, cognitive functioning, language, adaptive skills, behavior and mental health, assessment and diagnosis, age-related cognitive decline, and medical issues related to the neuropsychological phenotype and neuroimaging.
trisomy 21 --- decoding --- vocabulary --- letters --- phonological awareness --- down syndrome --- fluency --- disfluency --- co-occurrence --- comorbidity --- language --- Down syndrome --- social cognition --- social behavior --- measurement --- children --- attention --- audiovisual processing --- communicative abilities in infants --- Trisomy 21 --- independence --- transition to adulthood --- proxy-report --- regression --- Alzheimer’s disease --- biomarkers --- dementia --- cognition --- functional independence --- neuropsychological assessment --- primary care --- screening --- early regression --- idiopathic regression --- depression --- selective serotonin reuptake inhibitor --- mild cognitive impairment --- cognitive decline --- neuropsychological tests --- cognitive function --- early-onset Alzheimer disease --- late-onset Alzheimer disease --- hypothyroidism --- thyroid autoantibodies --- TSH --- Free T4 --- APOE Ɛ4 --- autism spectrum disorder --- co-occurring --- prevalence --- n/a --- Alzheimer's disease
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Depressive Disorder --- Anxiety Disorders --- Serotonin Uptake Inhibitors --- Depression, Mental --- Anxiety --- Serotonin uptake inhibitors --- Antidepressants --- Troubles affectifs --- drugtherapy. --- drug therapy. --- therapeutic use. --- Chemotherapy. --- Therapeutic use --- Effectiveness. --- Chimiothérapie --- drug therapy --- therapeutic use --- Chimiothérapie --- 5-HT uptake inhibitors --- 5-Hydroxytryptamine uptake inhibitors --- Inhibitors, Serotonic uptake --- Reuptake inhibitors, Serotonin --- Serotonin reuptake inhibitors --- Uptake inhibitors, Serotonin --- Neurotransmitter uptake inhibitors --- Angst --- Anxieties --- Anxiousness --- Emotions --- Stress (Psychology) --- Agitation (Psychology) --- Fear --- Worry --- Antidepressive agents --- Energizers, Psychic --- Psychic energizers --- Psychotropic drugs --- Effectiveness --- Chemotherapy --- Therapeutic use&delete& --- Selective Serotonin Reuptake Inhibitors --- Inhibitors, 5-HT Uptake --- Inhibitors, 5-Hydroxytryptamine Uptake --- Inhibitors, Serotonin Reuptake --- Inhibitors, Serotonin Uptake --- Reuptake Inhibitors, Serotonin --- Uptake Inhibitors, 5-HT --- Uptake Inhibitors, 5-Hydroxytryptamine --- Uptake Inhibitors, Serotonin --- 5-HT Uptake Inhibitor --- 5-HT Uptake Inhibitors --- 5-Hydroxytryptamine Uptake Inhibitor --- 5-Hydroxytryptamine Uptake Inhibitors --- SSRIs --- Selective Serotonin Reuptake Inhibitor --- Serotonin Reuptake Inhibitor --- Serotonin Reuptake Inhibitors --- Serotonin Uptake Inhibitor --- Inhibitor, 5-HT Uptake --- Inhibitor, 5-Hydroxytryptamine Uptake --- Inhibitor, Serotonin Reuptake --- Inhibitor, Serotonin Uptake --- Reuptake Inhibitor, Serotonin --- Uptake Inhibitor, 5-HT --- Uptake Inhibitor, 5-Hydroxytryptamine --- Uptake Inhibitor, Serotonin --- Serotonin Plasma Membrane Transport Proteins --- Serotonin Antagonists --- Serotonin Syndrome --- antagonists & inhibitors
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Down syndrome (DS), caused by the triplication of chromosome 21, is the most common genetic cause of intellectual disability (ID). Individuals with DS commonly exhibit unique neuropsychological profiles that emerge during specific developmental stages across the lifespan, often characterized by early developmental delay, cognitive strengths and weaknesses, behavior and mental health issues, and age-related cognitive decline, frequently resulting in early-onset Alzheimer’s disease. These profiles are unique compared to other individuals with ID and reflect the genetic mechanisms and neuroanatomic features underlying the distinct neuropsychological phenotype associated with DS. This Special Issue aims to highlight the recent advancements in understanding the neuropsychological phenotype associated with DS across the lifespan. The lifespan perspective will cover four developmental stages: (1) early childhood; (2) school age; (3) young adulthood, and (4) older adulthood. Authors contributed cutting-edge original research studies and comprehensive reviews that address a broad range of topics related to DS, including early developmental trajectories, cognitive functioning, language, adaptive skills, behavior and mental health, assessment and diagnosis, age-related cognitive decline, and medical issues related to the neuropsychological phenotype and neuroimaging.
Medicine --- Neurosciences --- trisomy 21 --- decoding --- vocabulary --- letters --- phonological awareness --- down syndrome --- fluency --- disfluency --- co-occurrence --- comorbidity --- language --- Down syndrome --- social cognition --- social behavior --- measurement --- children --- attention --- audiovisual processing --- communicative abilities in infants --- Trisomy 21 --- independence --- transition to adulthood --- proxy-report --- regression --- Alzheimer's disease --- biomarkers --- dementia --- cognition --- functional independence --- neuropsychological assessment --- primary care --- screening --- early regression --- idiopathic regression --- depression --- selective serotonin reuptake inhibitor --- mild cognitive impairment --- cognitive decline --- neuropsychological tests --- cognitive function --- early-onset Alzheimer disease --- late-onset Alzheimer disease --- hypothyroidism --- thyroid autoantibodies --- TSH --- Free T4 --- APOE Ɛ4 --- autism spectrum disorder --- co-occurring --- prevalence --- trisomy 21 --- decoding --- vocabulary --- letters --- phonological awareness --- down syndrome --- fluency --- disfluency --- co-occurrence --- comorbidity --- language --- Down syndrome --- social cognition --- social behavior --- measurement --- children --- attention --- audiovisual processing --- communicative abilities in infants --- Trisomy 21 --- independence --- transition to adulthood --- proxy-report --- regression --- Alzheimer's disease --- biomarkers --- dementia --- cognition --- functional independence --- neuropsychological assessment --- primary care --- screening --- early regression --- idiopathic regression --- depression --- selective serotonin reuptake inhibitor --- mild cognitive impairment --- cognitive decline --- neuropsychological tests --- cognitive function --- early-onset Alzheimer disease --- late-onset Alzheimer disease --- hypothyroidism --- thyroid autoantibodies --- TSH --- Free T4 --- APOE Ɛ4 --- autism spectrum disorder --- co-occurring --- prevalence
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Development provides an especially sensitive window whereby environmental contaminants can have significant and lasting effects on the morphology and function of many organs and systems. The importance of understanding developmental effects of environmental contaminants extends not only to developmental stages, but also to encompass the hypotheses of the developmental or fetal origins of adult disease. Such effects of environmental contaminants during development extend to health outcomes that can persist in adulthood, first become apparent in adulthood, or manifest in adulthood but only after a second hit/stressor. The diverse nature of possible environmental contaminants, ranging from persistent organic pollutants to emerging contaminants of concern, along with the diverse range of health implications, including autism, diabetes, cancer, infertility, and lower urinary tract function, make understanding developmental effects of environmental contaminants an ever growing and important field of study.This Special Issue aims to explore a variety of topics in line with the aims and scope of Toxics. Specifically, topics related to the developmental effects of environmental contaminants and/or their metabolites on the molecular, cellular, tissue, organ, organ system or organism, including mechanisms of toxicity, metabolism, risk assessment and management, as well as multiple stressor impacts in the context of aging or disease progression following developmental exposures.
Medicine --- Medical toxicology --- arsenic --- synaptic transmission --- long-term potentiation --- hippocampus --- development --- lower urinary tract --- bladder --- inflammation --- POPs --- developmental basis of adult disease --- multigenerational --- toxicants --- bronchopulmonary dysplasia --- therapeutics --- lung development --- selective serotonin reuptake inhibitor --- perinatal mortality --- neonatal morbidity --- fluoxetine --- sertraline --- endocrine-disrupting chemicals (EDC) --- Aroclor 1221 (A1221) --- PCBs --- vinclozolin --- social behavior --- sex differences --- transgenerational --- epigenetic --- endocrine-disrupting chemical (EDC) --- polychlorinated biphenyl (PCB) --- mating behavior --- paced mating --- ultrasonic vocalization (USV) --- estradiol --- triclosan --- triclocarbon --- detergents --- 4-nonylphenol --- Danio rerio --- zebrafish --- environmental toxicity --- aquatic environment --- ground water chemicals --- lower urinary tract dysfunction --- lower urinary tract symptoms --- BPH --- prostate --- axonal growth --- developmental neurotoxicity --- neuronal morphogenesis --- PBDE --- reactive oxygen species --- thyroid hormone --- pesticides --- prebiotic --- intestinal dysbiosis --- perigestational --- dysmetabolism --- risk factor --- behavior --- chemical screening --- literature comparison --- developmental toxicity --- negative control --- positive control --- rapid testing --- PFAS --- PFAS mixtures --- epigenetics --- microglia --- valproic acid --- primary motor cortex
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