Journal articles: 'Developmental biology/neurodevelopment'

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Coutinho-Budd, Jaeda C., and Heather T. Broihier. "Pyroptosis Takes Aim at Neurodevelopment." Developmental Cell 53, no. 5 (June 2020): 498–99. http://dx.doi.org/10.1016/j.devcel.2020.05.013.

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Armstrong, F. Daniel, T. David Elkin, R. Clark Brown, Penny Glass, Renee C. Rees, Winfred C. Wang, and The Baby HUG Investigators. "Neurodevelopment in Infants with Sickle Cell Anemia: Baseline Data from the Baby HUG Trial." Blood 112, no. 11 (November 16, 2008): 713. http://dx.doi.org/10.1182/blood.v112.11.713.713.

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Abstract Delays and deficits in neurodevelopment are known complications of sickle cell anemia (SCA) in young children1. Hydroxyurea is a chemotherapeutic agent that increases production of fetal hemoglobin, and has proven effective in reducing pain and other SCA-related complications in adults, adolescents, and school-age children. To determine whether treatment with hydroxyurea for 24 months would benefit infants with SCA, the NHLBI initiated a multi-center, randomized, double-blind, placebo-controlled clinical trial (NCT00006400) in 2003 (BABY HUG). After screening 233 infants for eligibility, 193 infants 9 to 17 months of age from 14 participating institutions were randomized. While the primary outcomes for BABY HUG are spleen and kidney function, neurodevelopment is an important safety assessment and a secondary outcome. Two hundred and seven (male=89, female = 117) infants were administered the Bayley Scales of Infant Development-2nd Edition (BSID-II) by qualified psychological examiners during the screening phase of the trial. The infants also completed a transcranial Doppler ultrasound (TCD) to determine flow velocity in seven ascending arteries of the brain. The analyses for this report focused on the relationships between neurodevelopmental function on the BSID-II, age at study entry and TCD flow velocities. Overall the mean neurodevelopmental function of the sample was in the average range (mean Motor Developmental Index= 96.8; mean Mental Developmental Index = 96.3). Age at study entry (continuous and categorical) was significantly correlated with the Mental Scale of the BSID-II (p=0.0042, p=0.0001, respectively). On average, a child’s Mental Developmental Index (MDI) decreased by 0.75 for every one month increase in age. Age (categorical) was also significantly associated with the Motor Scale of the BSID (p=0.0255). TCD velocity has been shown to be a sensitive indicator of existing and future risk for central nervous system (CNS) events in children with SCA. In children age 2–16 years, flow velocities over 200mm/ sec are associated with significant stroke risk; flow velocities between 170–200 mm/sec are associated with potential risk for neurodevelopmental deficits. Early associations between TCD and neurodevelopment could be considered important clinical indicators of risk for future CNS events. BSID Mental Scale scores were significantly associated with the maximum (of left or right) flow velocity in the M-1 artery (p=0.04) and the Behavior Rating Scale scores were significantly associated with the dICA velocity (p=0.008). In both of these cases, higher flow velocity was associated with poorer neurodevelopmental function. These results reflect the function of a large group of infants and toddlers with SCA prior to the initiation of any treatment targeting the CNS. Although the overall function of the group was in the average range, it is concerning to find strong relationships between increasing age at enrollment and decreasing MDI and between higher TCD flow velocity and decreased neurodevelopmental function in these very young children. The importance of early screening and perhaps sequential assessment of infants with both TCD and neurodevelopmental assessments is raised by these findings, as is the importance of continuing efforts to determine whether interventions, such as early HU therapy, might favorably impact the CNS complications of this disease that affect neurodevelopment.

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Zapata-Muñoz, Juan, Beatriz Villarejo-Zori, Pablo Largo-Barrientos, and Patricia Boya. "Towards a better understanding of the neuro-developmental role of autophagy in sickness and in health." Cell Stress 5, no. 7 (July 12, 2021): 99–118. http://dx.doi.org/10.15698/cst2021.07.253.

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Autophagy is a critical cellular process by which biomolecules and cellular organelles are degraded in an orderly manner inside lysosomes. This process is particularly important in neurons: these post-mitotic cells cannot divide or be easily replaced and are therefore especially sensitive to the accumulation of toxic proteins and damaged organelles. Dysregulation of neuronal autophagy is well documented in a range of neurodegenerative diseases. However, growing evidence indicates that autophagy also critically contributes to neurodevelopmental cellular processes, including neurogenesis, maintenance of neural stem cell homeostasis, differentiation, metabolic reprogramming, and synaptic remodelling. These findings implicate autophagy in neurodevelopmental disorders. In this review we discuss the current understanding of the role of autophagy in neurodevelopment and neurodevelopmental disorders, as well as currently available tools and techniques that can be used to further investigate this association.

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Norkett, Rosalind, Wen Lu, and Vladimir I. Gelfand. "Repurposing Kinetochore Microtubule Attachment Machinery in Neurodevelopment." Developmental Cell 48, no. 6 (March 2019): 746–48. http://dx.doi.org/10.1016/j.devcel.2019.03.004.

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Obst, Stefanie, Josephine Herz, Miguel A. Alejandre Alcazar, Stefanie Endesfelder, Marius A. Möbius, Mario Rüdiger, Ursula Felderhoff-Müser, and Ivo Bendix. "Perinatal Hyperoxia and Developmental Consequences on the Lung-Brain Axis." Oxidative Medicine and Cellular Longevity 2022 (February 24, 2022): 1–17. http://dx.doi.org/10.1155/2022/5784146.

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Approximately 11.1% of all newborns worldwide are born preterm. Improved neonatal intensive care significantly increased survival rates over the last decades but failed to reduce the risk for the development of chronic lung disease (i.e., bronchopulmonary dysplasia (BPD)) and impaired neurodevelopment (i.e., encephalopathy of prematurity (EoP)), two major long-term sequelae of prematurity. Premature infants are exposed to relative hyperoxia, when compared to physiological in-utero conditions and, if needed to additional therapeutic oxygen supplementation. Both are associated with an increased risk for impaired organ development. Since the detrimental effects of hyperoxia on the immature retina are known for many years, lung and brain have come into focus in the last decade. Hyperoxia-induced excessive production of reactive oxygen species leading to oxidative stress and inflammation contribute to pulmonary growth restriction and abnormal neurodevelopment, including myelination deficits. Despite a large body of studies, which unraveled important pathophysiological mechanisms for both organs at risk, the majority focused exclusively either on lung or on brain injury. However, considering that preterm infants suffering from BPD are at higher risk for poor neurodevelopmental outcome, an interaction between both organs seems plausible. This review summarizes recent findings regarding mechanisms of hyperoxia-induced neonatal lung and brain injury. We will discuss common pathophysiological pathways, which potentially link both injured organ systems. Furthermore, promises and needs of currently suggested therapies, including pharmacological and regenerative cell-based treatments for BPD and EoP, will be emphasized. Limited therapeutic approaches highlight the urgent need for a better understanding of the mechanisms underlying detrimental effects of hyperoxia on the lung-brain axis in order to pave the way for the development of novel multimodal therapies, ideally targeting both severe preterm birth-associated complications.

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Gomes, Ana Rita, Nasim Bahram Sangani, Tiago G. Fernandes, M. Margarida Diogo, Leopold M. G. Curfs, and Chris P. Reutelingsperger. "Extracellular Vesicles in CNS Developmental Disorders." International Journal of Molecular Sciences 21, no. 24 (December 11, 2020): 9428. http://dx.doi.org/10.3390/ijms21249428.

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The central nervous system (CNS) is the most complex structure in the body, consisting of multiple cell types with distinct morphology and function. Development of the neuronal circuit and its function rely on a continuous crosstalk between neurons and non-neural cells. It has been widely accepted that extracellular vesicles (EVs), mainly exosomes, are effective entities responsible for intercellular CNS communication. They contain membrane and cytoplasmic proteins, lipids, non-coding RNAs, microRNAs and mRNAs. Their cargo modulates gene and protein expression in recipient cells. Several lines of evidence indicate that EVs play a role in modifying signal transduction with subsequent physiological changes in neurogenesis, gliogenesis, synaptogenesis and network circuit formation and activity, as well as synaptic pruning and myelination. Several studies demonstrate that neural and non-neural EVs play an important role in physiological and pathological neurodevelopment. The present review discusses the role of EVs in various neurodevelopmental disorders and the prospects of using EVs as disease biomarkers and therapeutics.

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Lauter, Gilbert, Iris Söll, and Giselbert Hauptmann. "13-P133 PACAP in zebrafish neurodevelopment." Mechanisms of Development 126 (August 2009): S235. http://dx.doi.org/10.1016/j.mod.2009.06.606.

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Carvill, Gemma L., and Heather C. Mefford. "Poison exons in neurodevelopment and disease." Current Opinion in Genetics & Development 65 (December 2020): 98–102. http://dx.doi.org/10.1016/j.gde.2020.05.030.

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Chesnut, Megan, Thomas Hartung, Helena Hogberg, and David Pamies. "Human Oligodendrocytes and Myelin In Vitro to Evaluate Developmental Neurotoxicity." International Journal of Molecular Sciences 22, no. 15 (July 25, 2021): 7929. http://dx.doi.org/10.3390/ijms22157929.

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Neurodevelopment is uniquely sensitive to toxic insults and there are concerns that environmental chemicals are contributing to widespread subclinical developmental neurotoxicity (DNT). Increased DNT evaluation is needed due to the lack of such information for most chemicals in common use, but in vivo studies recommended in regulatory guidelines are not practical for the large-scale screening of potential DNT chemicals. It is widely acknowledged that developmental neurotoxicity is a consequence of disruptions to basic processes in neurodevelopment and that testing strategies using human cell-based in vitro systems that mimic these processes could aid in prioritizing chemicals with DNT potential. Myelination is a fundamental process in neurodevelopment that should be included in a DNT testing strategy, but there are very few in vitro models of myelination. Thus, there is a need to establish an in vitro myelination assay for DNT. Here, we summarize the routes of myelin toxicity and the known models to study this particular endpoint.

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Lu-Culligan, Alice, and Akiko Iwasaki. "The Role of Immune Factors in Shaping Fetal Neurodevelopment." Annual Review of Cell and Developmental Biology 36, no. 1 (October 6, 2020): 441–68. http://dx.doi.org/10.1146/annurev-cellbio-021120-033518.

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Fetal neurodevelopment in utero is profoundly shaped by both systemic maternal immunity and local processes at the maternal–fetal interface. Immune pathways are a critical participant in the normal physiology of pregnancy and perturbations of maternal immunity due to infections during this period have been increasingly linked to a diverse array of poor neurological outcomes, including diseases that manifest much later in postnatal life. While experimental models of maternal immune activation (MIA) have provided groundbreaking characterizations of the maternal pathways underlying pathogenesis, less commonly examined are the immune factors that serve pathogen-independent developmental functions in the embryo and fetus. In this review, we explore what is known about the in vivo role of immune factors in fetal neurodevelopment during normal pregnancy and provide an overview of how MIA perturbs the proper orchestration of this sequence of events. Finally, we discuss how the dysregulation of immune factors may contribute to the manifestation of a variety of neurological disorders.

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Zhao, Guoli, Asli Oztan, Yingzhi Ye, and Thomas L. Schwarz. "Kinetochore Proteins Have a Post-Mitotic Function in Neurodevelopment." Developmental Cell 48, no. 6 (March 2019): 873–82. http://dx.doi.org/10.1016/j.devcel.2019.02.003.

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Roko Rasin, Mladen, and Debra Silver. "The crossroads of RNA regulation and function in neurodevelopment." International Journal of Developmental Neuroscience 55, no. 1 (December 2016): 101. http://dx.doi.org/10.1016/j.ijdevneu.2016.11.002.

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Suárez‐Rodríguez, Marta, Cristina Azcona‐San Julián, and Valentín Alzina de Aguilar. "Hypothyroxinemia during pregnancy: the effect on neurodevelopment in the child." International Journal of Developmental Neuroscience 30, no. 6 (July 31, 2012): 435–38. http://dx.doi.org/10.1016/j.ijdevneu.2012.07.004.

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Dark, Callum, Jihane Homman-Ludiye, and Robert J. Bryson-Richardson. "The role of ADHD associated genes in neurodevelopment." Developmental Biology 438, no. 2 (June 2018): 69–83. http://dx.doi.org/10.1016/j.ydbio.2018.03.023.

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Litzinger, M. J., B. B. Grover, S. Saderup, and J. R. Abbott. "Voltage sensitive calcium channels mark a critical period in mouse neurodevelopment." International Journal of Developmental Neuroscience 11, no. 1 (February 1993): 17–24. http://dx.doi.org/10.1016/0736-5748(93)90031-8.

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Pearce, B. L., J. A. Owens, M. Dziadek, P. A. Grant, M. Wlodek, J. S. Robinson, and J. B. Pitcher. "162. THE EFFECT OF MATERNAL FOLIC ACID SUPPLEMENTATION THROUGHOUT PREGNANCY ON NEURODEVELOPMENT, MOTOR FUNCTION AND BEHAVIOUR OF PROGENY IN THE RAT." Reproduction, Fertility and Development 21, no. 9 (2009): 80. http://dx.doi.org/10.1071/srb09abs162.

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Background: Maternal folic acid supplementation (mFAS) during early pregnancy is recommended to reduce the incidence of neural tube defects and has recently been associated with improved neurodevelopment in children. However, the effect on neurodevelopment of mFAS from before conception and throughout pregnancy is unknown. We examined the effect of mFAS throughout the gestational period on postnatal growth, neurodevelopment and early adult motor function and behaviour in rat offspring. Methods: Female Wistar Rats were fed either a control (folic acid 2mg/kg, n=6) or moderate mFAS diet (folic acid 6mg/kg, n=6) from two weeks before mating with Lewis males, until birth of progeny. Male and female progeny (Control=36, mFAS=36) were weighed on postnatal day (PD) 3, 7, 14, 21, 40 and 90, and underwent various tests between PD4 and 14: righting reflex, palm-grasp reflex, negative geotaxis, forelimb hanging, ascent test and eye opening. Locomotor/ exploratory behaviour, motor coordination and anxiety were assessed using an open field test (PD52), rotarod (PD55) and elevated plus maze (PD58) (Control=24, mFAS=24). Results: mFAS did not alter maternal weight gain, litter-size at birth or progeny growth between PD3-90. mFAS tended to increase righting reflex time (p=0.057) and impair ascent ability (p=0.085). Negative geotaxis time was reduced at PD7 but not later (Diet x Age p=0.051). mFAS increased the proportion of progeny with eyes open at PD14 (p=0.008) and tended to increase forelimb hanging time(p=0.097). mFAS did not alter motor learning/function (rotarod), but increased ambulatory and exploratory behaviour (open field test; p=0.027). Conclusions: mFAS delays some early aspects of neurodevelopment including neonatal postural reflex maturation and proprioceptive/vestibular function, but accelerates others such as eye opening. However, the open field test indicated that mFAS improved the offspring's locomotion and exploratory behaviours in adulthood. Further studies will differentiate the neurodevelopmental effects of mFAS around conception from gestation-long mFAS.

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Pinazo-Durán, Maria D., Sheila Pons-Vázquez, Roberto Gallego-Pinazo, Carmen Galbis Estrada, Vicente Zanón-Moreno, Vicente Vila Bou, and Pedro Sanz Solana. "Thyroid hormone deficiency disrupts rat eye neurodevelopment." Brain Research 1392 (May 2011): 16–26. http://dx.doi.org/10.1016/j.brainres.2011.04.005.

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Flaherty, Erin, and Tom Maniatis. "The role of clustered protocadherins in neurodevelopment and neuropsychiatric diseases." Current Opinion in Genetics & Development 65 (December 2020): 144–50. http://dx.doi.org/10.1016/j.gde.2020.05.041.

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Klocke, Carolyn, and Pamela J. Lein. "Evidence Implicating Non-Dioxin-Like Congeners as the Key Mediators of Polychlorinated Biphenyl (PCB) Developmental Neurotoxicity." International Journal of Molecular Sciences 21, no. 3 (February 4, 2020): 1013. http://dx.doi.org/10.3390/ijms21031013.

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Despite being banned from production for decades, polychlorinated biphenyls (PCBs) continue to pose a significant risk to human health. This is due to not only the continued release of legacy PCBs from PCB-containing equipment and materials manufactured prior to the ban on PCB production, but also the inadvertent production of PCBs as byproducts of contemporary pigment and dye production. Evidence from human and animal studies clearly identifies developmental neurotoxicity as a primary endpoint of concern associated with PCB exposures. However, the relative role(s) of specific PCB congeners in mediating the adverse effects of PCBs on the developing nervous system, and the mechanism(s) by which PCBs disrupt typical neurodevelopment remain outstanding questions. New questions are also emerging regarding the potential developmental neurotoxicity of lower chlorinated PCBs that were not present in the legacy commercial PCB mixtures, but constitute a significant proportion of contemporary human PCB exposures. Here, we review behavioral and mechanistic data obtained from experimental models as well as recent epidemiological studies that suggest the non-dioxin-like (NDL) PCBs are primarily responsible for the developmental neurotoxicity associated with PCBs. We also discuss emerging data demonstrating the potential for non-legacy, lower chlorinated PCBs to cause adverse neurodevelopmental outcomes. Molecular targets, the relevance of PCB interactions with these targets to neurodevelopmental disorders, and critical data gaps are addressed as well.

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Setia, Harpreet, and Alysson R. Muotri. "Brain organoids as a model system for human neurodevelopment and disease." Seminars in Cell & Developmental Biology 95 (November 2019): 93–97. http://dx.doi.org/10.1016/j.semcdb.2019.03.002.

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Vargas, Lina, and Alejandra Alvarez. "P73 and P63: The siblings that work together in neurodevelopment." Cell Cycle 14, no. 23 (December 2, 2015): 3671–72. http://dx.doi.org/10.1080/15384101.2015.1112615.

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Lupu, Diana, Patrik Andersson, Carl-Gustaf Bornehag, Barbara Demeneix, Ellen Fritsche, Chris Gennings, Walter Lichtensteiger, et al. "The ENDpoiNTs Project: Novel Testing Strategies for Endocrine Disruptors Linked to Developmental Neurotoxicity." International Journal of Molecular Sciences 21, no. 11 (June 1, 2020): 3978. http://dx.doi.org/10.3390/ijms21113978.

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Ubiquitous exposure to endocrine-disrupting chemicals (EDCs) has caused serious concerns about the ability of these chemicals to affect neurodevelopment, among others. Since endocrine disruption (ED)-induced developmental neurotoxicity (DNT) is hardly covered by the chemical testing tools that are currently in regulatory use, the Horizon 2020 research and innovation action ENDpoiNTs has been launched to fill the scientific and methodological gaps related to the assessment of this type of chemical toxicity. The ENDpoiNTs project will generate new knowledge about ED-induced DNT and aims to develop and improve in vitro, in vivo, and in silico models pertaining to ED-linked DNT outcomes for chemical testing. This will be achieved by establishing correlative and causal links between known and novel neurodevelopmental endpoints and endocrine pathways through integration of molecular, cellular, and organismal data from in vitro and in vivo models. Based on this knowledge, the project aims to provide adverse outcome pathways (AOPs) for ED-induced DNT and to develop and integrate new testing tools with high relevance for human health into European and international regulatory frameworks.

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Geschwind, Daniel H., and Joseph G. Gleeson. "Editorial overview: Neurodevelopment Diseases and Neurogenetics pivot towards mechanisms and therapies." Current Opinion in Genetics & Development 65 (December 2020): iii—vii. http://dx.doi.org/10.1016/j.gde.2020.09.001.

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Grissom, Nicola M., and Teresa M. Reyes. "Gestational overgrowth and undergrowth affect neurodevelopment: similarities and differences from behavior to epigenetics." International Journal of Developmental Neuroscience 31, no. 6 (November 27, 2012): 406–14. http://dx.doi.org/10.1016/j.ijdevneu.2012.11.006.

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Tadenev, A. L. D., G. C. Lopez, A. Wray, P. G. Fuerst, and R. W. Burgess. "ISDN2014_0301: The role of DSCAMs in neurodevelopment and visual function in the mouse." International Journal of Developmental Neuroscience 47, Part_A (December 2015): 91. http://dx.doi.org/10.1016/j.ijdevneu.2015.04.248.

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Brewer‐Smyth, Kathleen, Monica Cornelius, and Elisabeth Pickelsimer. "ISDN2014_0404: Childhood correlates of lifetime violent criminal behaviour: An epidemiological perspective on neurodevelopment." International Journal of Developmental Neuroscience 47, Part_A (December 2015): 121. http://dx.doi.org/10.1016/j.ijdevneu.2015.04.323.

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Stavoe, Andrea K. H., and Erika L. F. Holzbaur. "Autophagy in Neurons." Annual Review of Cell and Developmental Biology 35, no. 1 (October 6, 2019): 477–500. http://dx.doi.org/10.1146/annurev-cellbio-100818-125242.

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Autophagy is the major cellular pathway to degrade dysfunctional organelles and protein aggregates. Autophagy is particularly important in neurons, which are terminally differentiated cells that must last the lifetime of the organism. There are both constitutive and stress-induced pathways for autophagy in neurons, which catalyze the turnover of aged or damaged mitochondria, endoplasmic reticulum, other cellular organelles, and aggregated proteins. These pathways are required in neurodevelopment as well as in the maintenance of neuronal homeostasis. Here we review the core components of the pathway for autophagosome biogenesis, as well as the cell biology of bulk and selective autophagy in neurons. Finally, we discuss the role of autophagy in neuronal development, homeostasis, and aging and the links between deficits in autophagy and neurodegeneration.

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Douceau, Sara, Tanya Deutsch Guerrero, and Julien Ferent. "Establishing Hedgehog Gradients during Neural Development." Cells 12, no. 2 (January 5, 2023): 225. http://dx.doi.org/10.3390/cells12020225.

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A morphogen is a signaling molecule that induces specific cellular responses depending on its local concentration. The concept of morphogenic gradients has been a central paradigm of developmental biology for decades. Sonic Hedgehog (Shh) is one of the most important morphogens that displays pleiotropic functions during embryonic development, ranging from neuronal patterning to axon guidance. It is commonly accepted that Shh is distributed in a gradient in several tissues from different origins during development; however, how these gradients are formed and maintained at the cellular and molecular levels is still the center of a great deal of research. In this review, we first explored all of the different sources of Shh during the development of the nervous system. Then, we detailed how these sources can distribute Shh in the surrounding tissues via a variety of mechanisms. Finally, we addressed how disrupting Shh distribution and gradients can induce severe neurodevelopmental disorders and cancers. Although the concept of gradient has been central in the field of neurodevelopment since the fifties, we also describe how contemporary leading-edge techniques, such as organoids, can revisit this classical model.

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Andersen, Susan L., and Carryl P. Navalta. "Altering the course of neurodevelopment: a framework for understanding the enduring effects of psychotropic drugs." International Journal of Developmental Neuroscience 22, no. 5-6 (August 2004): 423–40. http://dx.doi.org/10.1016/j.ijdevneu.2004.06.002.

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Key, B. "[P2.04]: Using zebrafish to understand the neurodevelopment role of susceptibility genes for autism spectrum disorder." International Journal of Developmental Neuroscience 28, no. 8 (November 2010): 686–87. http://dx.doi.org/10.1016/j.ijdevneu.2010.07.134.

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García-González, Judit, Bruno de Quadros, William Havelange, Alistair J. Brock, and Caroline H. Brennan. "Behavioral Effects of Developmental Exposure to JWH-018 in Wild-Type and Disrupted in Schizophrenia 1 (disc1) Mutant Zebrafish." Biomolecules 11, no. 2 (February 19, 2021): 319. http://dx.doi.org/10.3390/biom11020319.

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Synthetic cannabinoids can cause acute adverse psychological effects, but the potential impact when exposure happens before birth is unknown. Use of synthetic cannabinoids during pregnancy may affect fetal brain development, and such effects could be moderated by the genetic makeup of an individual. Disrupted in schizophrenia 1 (DISC1) is a gene with important roles in neurodevelopment that has been associated with psychiatric disorders in pedigree analyses. Using zebrafish as a model, we investigated (1) the behavioral impact of developmental exposure to 3 μM 1-pentyl-3-(1-naphthoyl)-indole (JWH-018; a common psychoactive synthetic cannabinoid) and (2) whether disc1 moderates the effects of JWH-018. As altered anxiety responses are seen in several psychiatric disorders, we focused on zebrafish anxiety-like behavior. Zebrafish embryos were exposed to JWH-018 from one to six days post-fertilization. Anxiety-like behavior was assessed using forced light/dark and acoustic startle assays in larvae and novel tank diving in adults. Compared to controls, both acutely and developmentally exposed zebrafish larvae had impaired locomotion during the forced light/dark test, but anxiety levels and response to startle stimuli were unaltered. Adult zebrafish developmentally exposed to JWH-018 spent less time on the bottom of the tank, suggesting decreased anxiety. Loss-of-function in disc1 increased anxiety-like behavior in the tank diving assay but did not alter sensitivity to JWH-018. Results suggest developmental exposure to JWH-018 has a long-term behavioral impact in zebrafish, which is not moderated by disc1.

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Jiang, Jialong, Shasha Li, Yiqiao Wang, Xue Xiao, Yi Jin, Yilong Wang, Zeyong Yang, Shikai Yan, and Yuanhai Li. "Potential neurotoxicity of prenatal exposure to sevoflurane on offspring: Metabolomics investigation on neurodevelopment and underlying mechanism." International Journal of Developmental Neuroscience 62, no. 1 (August 24, 2017): 46–53. http://dx.doi.org/10.1016/j.ijdevneu.2017.08.001.

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Xu, Yanyi, Junru Liu, Yonghui Tian, Zuo Wang, Zan Song, Kemin Li, Shengxiang Zhang, and Haiyu Zhao. "Wnt/β-Catenin Signaling Pathway Is Strongly Implicated in Cadmium-Induced Developmental Neurotoxicity and Neuroinflammation: Clues from Zebrafish Neurobehavior and In Vivo Neuroimaging." International Journal of Molecular Sciences 23, no. 19 (September 28, 2022): 11434. http://dx.doi.org/10.3390/ijms231911434.

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Cadmium (Cd) is a toxic heavy metal and worldwide environmental pollutant which seriously threatens human health and ecosystems. It is easy to be adsorbed and deposited in organisms, exerting adverse effects on various organs including the brain. In a very recent study, making full use of a zebrafish model in both high-throughput behavioral tracking and live neuroimaging, we explored the potential developmental neurotoxicity of Cd2+ at environmentally relevant levels and identified multiple connections between Cd2+ exposure and neurodevelopmental disorders as well as microglia-mediated neuroinflammation, whereas the underlying neurotoxic mechanisms remained unclear. The canonical Wnt/β-catenin signaling pathway plays crucial roles in many biological processes including neurodevelopment, cell survival, and cell cycle regulation, as well as microglial activation, thereby potentially presenting one of the key targets of Cd2+ neurotoxicity. Therefore, in this follow-up study, we investigated the implication of the Wnt/β-catenin signaling pathway in Cd2+-induced developmental disorders and neuroinflammation and revealed that environmental Cd2+ exposure significantly affected the expression of key factors in the zebrafish Wnt/β-catenin signaling pathway. In addition, pharmacological intervention of this pathway via TWS119, which can increase the protein level of β-catenin and act as a classical activator of the Wnt signaling pathway, could significantly repress the Cd2+-induced cell cycle arrest and apoptosis, thereby attenuating the inhibitory effects of Cd2+ on the early development, behavior, and activity, as well as neurodevelopment of zebrafish larvae to a certain degree. Furthermore, activation and proliferation of microglia, as well as the altered expression profiles of genes associated with neuroimmune homeostasis triggered by Cd2+ exposure could also be significantly alleviated by the activation of the Wnt/β-catenin signaling pathway. Thus, this study provided novel insights into the cellular and molecular mechanisms of Cd2+ toxicity on the vertebrate central nervous system (CNS), which might be helpful in developing pharmacotherapies to mitigate the neurological disorders resulting from exposure to Cd2+ and many other environmental heavy metals.

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Bruckner, Joseph J., Sarah J. Stednitz, Max Z. Grice, Dana Zaidan, Michelle S. Massaquoi, Johannes Larsch, Alexandra Tallafuss, Karen Guillemin, Philip Washbourne, and Judith S. Eisen. "The microbiota promotes social behavior by modulating microglial remodeling of forebrain neurons." PLOS Biology 20, no. 11 (November 1, 2022): e3001838. http://dx.doi.org/10.1371/journal.pbio.3001838.

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Host-associated microbiotas guide the trajectory of developmental programs, and altered microbiota composition is linked to neurodevelopmental conditions such as autism spectrum disorder. Recent work suggests that microbiotas modulate behavioral phenotypes associated with these disorders. We discovered that the zebrafish microbiota is required for normal social behavior and reveal a molecular pathway linking the microbiota, microglial remodeling of neural circuits, and social behavior in this experimentally tractable model vertebrate. Examining neuronal correlates of behavior, we found that the microbiota restrains neurite complexity and targeting of forebrain neurons required for normal social behavior and is necessary for localization of forebrain microglia, brain-resident phagocytes that remodel neuronal arbors. The microbiota also influences microglial molecular functions, including promoting expression of the complement signaling pathway and the synaptic remodeling factor c1q. Several distinct bacterial taxa are individually sufficient for normal microglial and neuronal phenotypes, suggesting that host neuroimmune development is sensitive to a feature common among many bacteria. Our results demonstrate that the microbiota influences zebrafish social behavior by stimulating microglial remodeling of forebrain circuits during early neurodevelopment and suggest pathways for new interventions in multiple neurodevelopmental disorders.

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Pattwell, Siobhan, Sonali Arora, Nicholas Nuechterlein, Michael Zager, Keith Loeb, Patrick Cimino, Nikolas Holland, et al. "TMOD-30. NTRK2 SPLICE VARIANT, TRKB.T1, LINKS NEUROBIOLOGY, EMBRYONIC DEVELOPMENT, AND ONCOGENESIS." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi222. http://dx.doi.org/10.1093/neuonc/noab196.891.

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Abstract Temporally regulated alternative splicing choices are vital for proper development yet the wrong splice choice may be detrimental. Here we highlight a novel role for the neurotrophin receptor splice variant TrkB.T1 in neurodevelopment, embryogenesis, transformation, and oncogenesis across multiple tumor types in both humans and mice. TrkB.T1 is the predominant NTRK2 isoform across embryonic organogenesis and is highly expressed in a wide range of adult and pediatric tumors. Further, forced expression of TrkB.T1 causes multiple solid and non-solid tumors in mice in the context of tumor suppressor loss. These results highlight a unique role for the neurotrophin receptor splicing in development and oncogenesis and underscore the need for considering alternative splicing and transcript level data in neuroscience, developmental biology, and oncology research.

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Key, Brian. "Using zebrafish to understand the neurodevelopment role of susceptibility genes for autism spectrum disorder." Developmental Biology 344, no. 1 (August 2010): 526–27. http://dx.doi.org/10.1016/j.ydbio.2010.05.486.

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Grova, Nathalie, Henri Schroeder, Jean-Luc Olivier, and Jonathan D. Turner. "Epigenetic and Neurological Impairments Associated with Early Life Exposure to Persistent Organic Pollutants." International Journal of Genomics 2019 (January 14, 2019): 1–19. http://dx.doi.org/10.1155/2019/2085496.

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The incidence of neurodevelopmental and neurodegenerative diseases worldwide has dramatically increased over the last decades. Although the aetiology remains uncertain, evidence is now growing that exposure to persistent organic pollutants during sensitive neurodevelopmental periods such as early life may be a strong risk factor, predisposing the individual to disease development later in life. Epidemiological studies have associated environmentally persistent organic pollutant exposure to brain disorders including neuropathies, cognitive, motor, and sensory impairments; neurodevelopmental disorders such as autism spectrum disorder (ASD) and attention-deficit hyperactivity disorder (ADHD); and neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS). In many ways, this expands the classical “Developmental Origins of Health and Disease” paradigm to include exposure to pollutants. This model has been refined over the years to give the current “three-hit” model that considers the individual’s genetic factors as a first “hit.” It has an immediate interaction with the early-life exposome (including persistent organic pollutants) that can be considered to be a second “hit.” Together, these first two “hits” produce a quiescent or latent phenotype, most probably encoded in the epigenome, which has become susceptible to a third environmental “hit” in later life. It is only after the third “hit” that the increased risk of disease symptoms is crystallised. However, if the individual is exposed to a different environment in later life, they would be expected to remain healthy. In this review, we examine the effect of exposure to persistent organic pollutants and particulate matters in early life and the relationship to subsequent neurodevelopmental and neurodegenerative disorders. The roles of those environmental factors which may affect epigenetic DNA methylation and therefore influence normal neurodevelopment are then evaluated.

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Hood, Veronica L., Ralph Berger, Robert Freedman, and Amanda J. Law. "Transcription of PIK3CD in human brain and schizophrenia: regulation by proinflammatory cytokines." Human Molecular Genetics 28, no. 19 (May 14, 2019): 3188–98. http://dx.doi.org/10.1093/hmg/ddz144.

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Abstract PIK3CD encodes the phosphoinositide 3-kinase (PI3K) catalytic subunit, p110δ, a lipid kinase linked to neurodevelopmental disorders, including schizophrenia (SZ). PIK3CD is regulated at the transcript level through alternate use of 5' untranslated exons (UTRs), promoters, and proinflammatory cytokines. Increases in global PIK3CD expression and downregulation by neuroleptics are observed in SZ, and preclinical efficacy of a p110δ-selective inhibitor is seen in rodent models of risk. Here, we cloned PIK3CD alternative transcripts in human brain and evaluated temporal- and tissue-specific expression. We quantified PIK3CD transcripts in B-lymphoblastoid cells from patients with SZ and examined 5' UTR transcriptional regulation by tumor necrosis factor α (TNFα) and interleukin-1β (IL1β) in patient-derived fibroblasts. We report that PIK3CD transcripts are differentially expressed in human brain in a developmental-specific manner. Transcripts encoding 5' UTRs -2A and alternative exon -1 (Alt1), P37 and AS1 and AS2 were increased in SZ. Alt1, P37, and AS2 were also preferentially expressed in fetal brain, and all transcripts were regulated by TNFα and IL1β. Our findings provide novel insight into the complexity of PIK3CD regulation in human brain, implicate PIK3CD in human neurodevelopment, and identify isoform-specific disruption in SZ.

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Rosa, Filip, Ashutosh Dhingra, Betül Uysal, G. Dulini C. Mendis, Heidi Loeffler, Gina Elsen, Stephan Mueller, et al. "In Vitro Differentiated Human Stem Cell-Derived Neurons Reproduce Synaptic Synchronicity Arising during Neurodevelopment." Stem Cell Reports 15, no. 1 (July 2020): 22–37. http://dx.doi.org/10.1016/j.stemcr.2020.05.015.

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Igonina, Tatyana N., Diana S. Ragaeva, Maria A. Tikhonova, Olga M. Petrova, Yuri E. Herbeck, Irina N. Rozhkova, Tamara G. Amstislavskaya, and Sergey Ya Amstislavsky. "Neurodevelopment and behavior in neonatal OXYS rats with genetically determined accelerated senescence." Brain Research 1681 (February 2018): 75–84. http://dx.doi.org/10.1016/j.brainres.2017.12.021.

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Falugi, Carla, Maria Lammerding-Koppel, and Maria Grazia Aluigi. "Sea urchin development: An alternative model for mechanistic understanding of neurodevelopment and neurotoxicity." Birth Defects Research Part C: Embryo Today: Reviews 84, no. 3 (September 2008): 188–203. http://dx.doi.org/10.1002/bdrc.20132.

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Nazar, Ada Paula, María José Delgado, and Andrés Lavore. "Empty-spiracles is maternally expressed and essential for neurodevelopment and early embryo determination in Rhodnius prolixus." Developmental Biology 490 (October 2022): 144–54. http://dx.doi.org/10.1016/j.ydbio.2022.08.001.

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Xu, Jing, R. Mathena, Michael Xu, YuChia Wang, CheJui Chang, Yiwen Fang, Pengbo Zhang, and C. Mintz. "Early Developmental Exposure to General Anesthetic Agents in Primary Neuron Culture Disrupts Synapse Formation via Actions on the mTOR Pathway." International Journal of Molecular Sciences 19, no. 8 (July 26, 2018): 2183. http://dx.doi.org/10.3390/ijms19082183.

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Human epidemiologic studies and laboratory investigations in animal models suggest that exposure to general anesthetic agents (GAs) have harmful effects on brain development. The mechanism underlying this putative iatrogenic condition is not clear and there are currently no accepted strategies for prophylaxis or treatment. Recent evidence suggests that anesthetics might cause persistent deficits in synaptogenesis by disrupting key events in neurodevelopment. Using an in vitro model consisting of dissociated primary cultured mouse neurons, we demonstrate abnormal pre- and post-synaptic marker expression after a clinically-relevant isoflurane anesthesia exposure is conducted during neuron development. We find that pharmacologic inhibition of the mechanistic target of rapamycin (mTOR) pathway can reverse the observed changes. Isoflurane exposure increases expression of phospho-S6, a marker of mTOR pathway activity, in a concentration-dependent fashion and this effect occurs throughout neuronal development. The mTOR 1 complex (mTORC1) and the mTOR 2 complex (mTORC2) branches of the pathway are both activated by isoflurane exposure and this is reversible with branch-specific inhibitors. Upregulation of mTOR is also seen with sevoflurane and propofol exposure, suggesting that this mechanism of developmental anesthetic neurotoxicity may occur with all the commonly used GAs in pediatric practice. We conclude that GAs disrupt the development of neurons during development by activating a well-defined neurodevelopmental disease pathway and that this phenotype can be reversed by pharmacologic inhibition.

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Brace, E. J., Kow Essuman, Xianrong Mao, John Palucki, Yo Sasaki, Jeff Milbrandt, and Aaron DiAntonio. "Distinct developmental and degenerative functions of SARM1 require NAD+ hydrolase activity." PLOS Genetics 18, no. 6 (June 23, 2022): e1010246. http://dx.doi.org/10.1371/journal.pgen.1010246.

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SARM1 is the founding member of the TIR-domain family of NAD+ hydrolases and the central executioner of pathological axon degeneration. SARM1-dependent degeneration requires NAD+ hydrolysis. Prior to the discovery that SARM1 is an enzyme, SARM1 was studied as a TIR-domain adaptor protein with non-degenerative signaling roles in innate immunity and invertebrate neurodevelopment, including at the Drosophila neuromuscular junction (NMJ). Here we explore whether the NADase activity of SARM1 also contributes to developmental signaling. We developed transgenic Drosophila lines that express SARM1 variants with normal, deficient, and enhanced NADase activity and tested their function in NMJ development. We find that NMJ overgrowth scales with the amount of NADase activity, suggesting an instructive role for NAD+ hydrolysis in this developmental signaling pathway. While degenerative and developmental SARM1 signaling share a requirement for NAD+ hydrolysis, we demonstrate that these signals use distinct upstream and downstream mechanisms. These results identify SARM1-dependent NAD+ hydrolysis as a heretofore unappreciated component of developmental signaling. SARM1 now joins sirtuins and Parps as enzymes that regulate signal transduction pathways via mechanisms that involve NAD+ cleavage, greatly expanding the potential scope of SARM1 TIR NADase functions.

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Yang, Guang, and Alex Shcheglovitov. "Probing disrupted neurodevelopment in autism using human stem cell‐derived neurons and organoids: An outlook into future diagnostics and drug development." Developmental Dynamics 249, no. 1 (October 2019): 6–33. http://dx.doi.org/10.1002/dvdy.100.

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Shallie, Philemon Dauda, and Thajasvarie Naicker. "The placenta as a window to the brain: A review on the role of placental markers in prenatal programming of neurodevelopment." International Journal of Developmental Neuroscience 73, no. 1 (January 8, 2019): 41–49. http://dx.doi.org/10.1016/j.ijdevneu.2019.01.003.

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Aguwa, Chi, Alicia D. Cannon, James F. Casella, Bruce K. Shapiro, and Eboni I. Lance. "Neurodevelopmental Screening in Young Children with Sickle Cell Disease." Blood 138, Supplement 1 (November 5, 2021): 2050. http://dx.doi.org/10.1182/blood-2021-152015.

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Abstract It is important to prioritize screening and surveillance for neurodevelopmental dysfunction in children with SCD because this vulnerable population is at higher risk for neurological complications including stroke, silent cerebral infarction, and neurodevelopmental disorders (NDD) such as language disorders, attention deficit hyperactivity disorder, and autism spectrum disorder (ASD). The American Society of Hematology (ASH) and American Academy of Pediatrics (AAP) have published guidelines to accomplish this, as well as to improve quality of life for people with SCD and NDDs. Despite the recognition of the increased risk and the clinical guidelines, the co-occurrence rates of SCD and NDD remain lower than expected. We hypothesize that the risk of NDDs is lower than expected in children with SCD due to low rates of neurodevelopmental screening and surveillance among primary care providers and hematologists, particularly in young children. Therefore, we examined the frequency of neurodevelopmental screening and surveillance among young children with SCD and identified clinical characteristics of young children with SCD who did not receive appropriate neurodevelopmental screening and surveillance. We conducted a retrospective chart review using the clinic rosters of two affiliated inner-city hospitals with a pediatric hematology clinic and sickle cell neurodevelopmental clinic. Children under 5 years old with SCD confirmed by their hematologists who were not adopted or in foster care were included in the study. A total of 276 patients were identified and reviewed. NDD and ASD specific screenings were documented at the time of review, although participants may have been diagnosed later in life. Analyses were completed using chi squared test, Fisher exact test, t-test in Stata IC-15. Patients were screened by a variety of providers, most commonly pediatricians and hematologists (see Figure 1). Table 1a shows the characteristics of the SCD patients assessed/not assessed for appropriate neurodevelopment (ND) by their pediatrician and/or hematologist. A total of 214 participants qualified for study inclusion and 148 participants (70%) were assessed for neurodevelopment. Ages and Stages Questionnaire- 3 (32%) and other non-standardized screening tools (85%) were the most common tool used (see Table 2a). Of the ND assessed patients (N=148), 37 (25%) were diagnosed with NDDs (see Table 3a). Among the not assessed ND patients (N=66), 16 (24%) were diagnosed with NDDs. Table 1b shows the characteristics of the SCD patients assessed/not assessed specifically for ASD by their pediatrician and/or hematologist. A total of 207 participants qualified for study inclusion and 39 participants (19%) were assessed for ASD. Modified Checklist for Autism in Toddlers (92%) was the most utilized screening tool (see Table 2b). None of these patients had ASD. Of the ASD assessed patients (N=39), 9 (23%) were diagnosed with NDDs (see Table 3a). Among the not assessed ASD patients (N=168), 41 (24%) were diagnosed with NDDs. Children with SCD are being screened by their healthcare providers at a much lower rate than the general pediatric population. More specifically, many children with SCD were being screened for NDD, but not ASD. Among screened children, a majority were screened with non-standardized (or poorly documented) tools or outside the age guidelines recommended by ASH and AAP (see Figure 2). Children among ND and ASD assessment groups exhibited similar percentages of NDD diagnosis, which may highlight disparities in screening and early detection of these disorders; NDDs may have also been diagnosed later in life these patients. Guidelines regarding developmental screening in pediatric SCD were released in mid-2020; given the short timeline, we did not expect to see changes in practice from this chart review. However, the AAP has guidelines for developmental surveillance and screening since 2004. Due to study design, limitations include lack of access to some data at the time of review, as patient medical records were switched to another electronic system. Additionally, standardized tools may have been used but not documented in patient charts. In conclusion, it is crucial to know the utility of these assessments in this vulnerable population. A future study could examine how the rates of screening and surveillance have changed since the guidelines release, using these data for comparison purposes. Figure 1 Figure 1. Disclosures Casella: Mast Pharmaceuticals (previously Adventrx Pharmaceuticals): Consultancy, Honoraria, Patents & Royalties. Lance: Novartis: Other: participated in research advisory board in 2020.

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Baracaldo-Santamaría, Daniela, María Gabriela Corrales-Hernández, Maria Camila Ortiz-Vergara, Valeria Cormane-Alfaro, Ricardo-Miguel Luque-Bernal, Carlos-Alberto Calderon-Ospina, and Juan-Fernando Cediel-Becerra. "Connexins and Pannexins: Important Players in Neurodevelopment, Neurological Diseases, and Potential Therapeutics." Biomedicines 10, no. 9 (September 9, 2022): 2237. http://dx.doi.org/10.3390/biomedicines10092237.

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Cell-to-cell communication is essential for proper embryonic development and its dysfunction may lead to disease. Recent research has drawn attention to a new group of molecules called connexins (Cxs) and pannexins (Panxs). Cxs have been described for more than forty years as pivotal regulators of embryogenesis; however, the exact mechanism by which they provide this regulation has not been clearly elucidated. Consequently, Cxs and Panxs have been linked to congenital neurodegenerative diseases such as Charcot-Marie-Tooth disease and, more recently, chronic hemichannel opening has been associated with adult neurodegenerative diseases (e.g., Alzheimer’s disease). Cell-to-cell communication via gap junctions formed by hexameric assemblies of Cxs, known as connexons, is believed to be a crucial component in developmental regulation. As for Panxs, despite being topologically similar to Cxs, they predominantly seem to form channels connecting the cytoplasm to the extracellular space and, despite recent research into Panx1 (Pannexin 1) expression in different regions of the brain during the embryonic phase, it has been studied to a lesser degree. When it comes to the nervous system, Cxs and Panxs play an important role in early stages of neuronal development with a wide span of action ranging from cellular migration during early stages to neuronal differentiation and system circuitry formation. In this review, we describe the most recent available evidence regarding the molecular and structural aspects of Cx and Panx channels, their role in neurodevelopment, congenital and adult neurological diseases, and finally propose how pharmacological modulation of these channels could modify the pathogenesis of some diseases.

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MacArthur, Ian C., and Meelad M. Dawlaty. "TET Enzymes and 5-Hydroxymethylcytosine in Neural Progenitor Cell Biology and Neurodevelopment." Frontiers in Cell and Developmental Biology 9 (February 18, 2021). http://dx.doi.org/10.3389/fcell.2021.645335.

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Studies of tissue-specific epigenomes have revealed 5-hydroxymethylcytosine (5hmC) to be a highly enriched and dynamic DNA modification in the metazoan nervous system, inspiring interest in the function of this epigenetic mark in neurodevelopment and brain function. 5hmC is generated by oxidation of 5-methylcytosine (5mC), a process catalyzed by the ten–eleven translocation (TET) enzymes. 5hmC serves not only as an intermediate in DNA demethylation but also as a stable epigenetic mark. Here, we review the known functions of 5hmC and TET enzymes in neural progenitor cell biology and embryonic and postnatal neurogenesis. We also discuss how TET enzymes and 5hmC regulate neuronal activity and brain function and highlight their implications in human neurodevelopmental and neurodegenerative disorders. Finally, we present outstanding questions in the field and envision new research directions into the roles of 5hmC and TET enzymes in neurodevelopment.

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Clarke, Taylor, Francesca E. Fernandez, and Paul A. Dawson. "Sulfation Pathways During Neurodevelopment." Frontiers in Molecular Biosciences 9 (April 14, 2022). http://dx.doi.org/10.3389/fmolb.2022.866196.

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Sulfate is an important nutrient that modulates a diverse range of molecular and cellular functions in mammalian physiology. Over the past 2 decades, animal studies have linked numerous sulfate maintenance genes with neurological phenotypes, including seizures, impaired neurodevelopment, and behavioral abnormalities. Despite sulfation pathways being highly conserved between humans and animals, less than one third of all known sulfate maintenance genes are clinically reportable. In this review, we curated the temporal and spatial expression of 91 sulfate maintenance genes in human fetal brain from 4 to 17 weeks post conception using the online Human Developmental Biology Resource Expression. In addition, we performed a systematic search of PubMed and Embase, identifying those sulfate maintenance genes linked to atypical neurological phenotypes in humans and animals. Those findings, together with a search of the Online Mendelian Inheritance in Man database, identified a total of 18 candidate neurological dysfunction genes that are not yet considered in clinical settings. Collectively, this article provides an overview of sulfate biology genes to inform future investigations of perturbed sulfate homeostasis associated with neurological conditions.

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Journal articles on the topic 'Developmental biology/neurodevelopment'

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