Relevant bibliographies by topics / Developmental biology/neurodevelopment

Academic literature on the topic 'Developmental biology/neurodevelopment'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Developmental biology/neurodevelopment.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Developmental biology/neurodevelopment"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Developmental biology/neurodevelopment"

1

Czerminski, Jan T. "Modeling Down Syndrome Neurodevelopment with Dosage Compensation." eScholarship@UMMS, 2019. https://escholarship.umassmed.edu/gsbs_diss/1037.

Full text
Abstract:
Due to their underlying genetic complexity, chromosomal disorders such as Down syndrome (DS), which is caused by trisomy 21, have long been understudied and continue to lack effective treatments. With over 200 genes on the extra chromosome, even the specific cell pathologies and pathways impacted in DS are not known, and it has not been considered a viable target for the burgeoning field of gene therapy. Recently, our lab demonstrated that the natural mechanism of dosage compensation can be harnessed to silence the trisomic chromosome in pluripotent cells. Using an inducible XIST transgene allows us to study the effects of trisomy in a tightly controlled system by comparing the same cells with either two or three active copies of chromosome 21. In addition, it raises the prospect that insertion of a single gene into a trisomic chromosome could potentially be developed in the future for “chromosome therapy”. This thesis aims to utilize this inducible system for dosage compensation to study the neurodevelopmental effects of trisomy 21 in vitro, and to answer basic epigenetic questions critical to the viability of chromosome silencing as a therapeutic approach. Foremost, for XIST to have any prospect as a therapeutic, and to strengthen its experimental utility, it must be able to initiate chromosome silencing beyond its natural context of pluripotency. Here I demonstrate that, contrary to the current literature, XIST is capable of initiating chromosome silencing in differentiated cells and producing fully dosage compensated DS neurons. Additionally, I show that silencing of the trisomic chromosome in neural stem cells enhances their terminal differentiation to neurons, and transcriptome analysis provides evidence of a specific pathway involved. Separate experiments utilize novel three-dimensional organoid technology and transcriptome analysis to model DS neurodevelopment in relation to isogenic euploid cells. Overall, this work demonstrates that dosage compensation provides a powerful experimental tool to examine early DS neurodevelopment, and establishes that XIST function does not require pluripotency, thereby overcoming a perceived obstacle to the potential of XIST as a therapeutic strategy for trisomy.
APA, Harvard, Vancouver, ISO, and other styles
2

Dai, Lu. "EFFECTS OF CHROMIUM ON MOUSE SPLENIC T LYMPHOCYTES AND EFFECTS OF ETHANOL EXPOSURE DURING EARLY NEURODEVELOPMENT ON BEHAVIORS IN MICE." UKnowledge, 2017. https://uknowledge.uky.edu/toxicology_etds/18.

Full text
Abstract:
The dissertation consists of three major projects with the focus on the immunotoxicity of chromium and the behavior disorders caused by early ETOH exposure respectively. Hexavalent chromium [Cr(VI)] is widely used in various industrial processes and has been recognized as a carcinogen. As the first line of host defense system, the immune system can be a primary target of Cr(VI). T cell population represents a major arm of the immune system that plays a critical role in host anti-tumor immunity. Dysfunction of T cells compromises host anti-tumor immunity resulting in oncogenesis. Using mouse splenic T cells as an in vitro model system, the present study assessed the effects of Cr(VI) on T cell functions, as the first step of our investigation of the mechanism underlying Cr(VI)-inhibited immunosurveillance and carcinogenesis. Our results showed that Cr(VI) decreased the viability of CD4+ and CD8+ T cells, inhibited T cell activation, functions, including cytokine release, and degranulation. Fetal ethanol (ETOH) exposure can damage the developing central nervous system and lead to cognitive and behavioral deficits, known as fetal alcohol spectrum disorders (FASD). The use of animal models, especially mouse models is essential for investigating the neurogenetic mechanism of fetal ETOH effects and screening pharmacotherapies against it, due to the extensive knowledge of mouse genetics. However, the availability of mouse model is limited. Via adopting various dosage, timing and administration routes of ETOH exposure, we developed two mouse models to assess behavioral or cognitive changes caused by fetal ETOH exposure in pre-weaning and adolescent period. Our results show that high dosage of ETOH exposure (4 g/kg) during PD 4-10 resulted in hyperactivity, disinhibition, and deficits in learning and memory in mouse offspring, which lays the groundwork for the future FASD research.
APA, Harvard, Vancouver, ISO, and other styles
3

Sears, James Cooper. "FoxO Regulates Microtubule Dynamics and Polarity to Promote Dendrite Branching in Drosophila Sensory Neurons." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1476705366788041.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Sarn, Nicholas Brian. "MICROGLIA PATHOLOGY: AN INHERENT FEATURE OF CONSTITUTIONAL PTEN DYSFUNCTION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1619526347351812.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Emerson, Sarah Elizabeth. "Neurodevelopmental Roles of Semaphorin6A/PlexinA2 Signaling in Zebrafish." ScholarWorks @ UVM, 2019. https://scholarworks.uvm.edu/graddis/1058.

Full text
Abstract:
ABSTRACT A multitude of complex cellular changes are required throughout development in order for a single cell to transform into a fully functioning organism. Cellular events including proliferation, migration, and differentiation have to be carefully controlled in order for development to proceed correctly. In order to study such dynamic processes, in vivo models are often utilized. Using the zebrafish (Danio rerio) as a model system, we have investigated the role of an axon guidance signaling pair, Semaphorin6A (Sema6A) and PlexinA2 (PlxnA2), in neurodevelopment. A previous investigation into the developmental expression patterns of sema6A and plxnA2 in zebrafish, revealed overlapping expression in the developing eye. At this early stage, the cells in the optic vesicles are undifferentiated retinal precursor cells (RPCs) and therefore do not require Sema/Plxn signaling for their canonical axon guidance role. To understand what the function of this early expression was, we knocked down both sema6a and plxna2 and observed 1) a loss of cohesion of RPCs within optic vesicles, and 2) a decrease in RPC proliferation (Ebert et al., 2014). Because these phenotypes were seen at an early stage and given that many developmental processes are dependent on genetic regulation, we hypothesized that Sema6A/PlxnA2 signaling could be regulating transcription of downstream target genes. To investigate this, we performed a microarray experiment and uncovered 58 differentially regulated genes (Emerson et al., 2017a). Prior to our study, it was not known that Sema/Plxn signaling led to changes in gene transcription. In an effort to understand the contribution of identified candidate genes to early sema6A/plxnA2 knockdown phenotypes, candidate genes with predicted functions in proliferation and migration were investigated. First, we show that rasl11b is important for regulation of RPC proliferation in the developing optic vesicles. Second, we show that shootin-1 is important in optic vesicle migration, retinal pigmented epithelium formation and optic tract patterning. Furthermore, PlxnA2 regulation of shootin-1 levels is important in sensory and motor axon patterning and branching in the peripheral nervous system. Belonging to a large family of proteins with the ability to cross talk, Semas and Plxns rely on spatially and temporally differential expression patterns to perform their tissue-specific roles. Here, we used in situ hybridization to comprehensively uncover the neuronal expression patterns of the PlxnA family in the early developing zebrafish (Emerson et al., 2017b). In addition, we present for the first time that zebrafish have two genes for PlxnA1, A1a and A1b, which show divergent expression patterns. Semas and Plxns are critical for many aspects of development and together, this body of work provides further insight into the downstream signaling mechanisms and roles of these essential developmental signaling proteins.
APA, Harvard, Vancouver, ISO, and other styles
6

Kim, Seol-Hee. "Acetaminophen Associated Neurotoxicity and its Relevance to Neurodevelopmental Disorders." Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6717.

Full text
Abstract:
Autism is a lifelong neurodevelopmental disorder. The etiology of autism still remains unclear due to the heterogeneous and complex nature of the disorder, however synergistic actions between genetic components and environmental factors have been suggested. Acetaminophen (APAP) is one of the most popular over-the-counter drugs that possess antipyretic and analgesic effects. It is considered a relatively safe and effective within therapeutic doses. Recently, early exposure to APAP has been suggested to be one of the underlying cause of autism. Children are often prescribed APAP to lessen fever or irritability after vaccination during the first year, and APAP may adversely affect the normal brain development. In order to better understand the association with APAP and autism, we used an inbred mouse strain BTBR T+tf/J (BTBR). BTBR exhibits behavioral deficits that mimic the core behavioral deficits of human autism. In the study, investigated 1) if BTBR mice showed differences in thiol biochemistry and EAAT3 levels in brain compared with C57BL/6J (C57) mice, 2) if early exposure to APAP induced behavioral changes worsening the autistic phenotypes of BTBR in adolescence, and 3) if APAP exposure in neonatal mice induced possible toxicity at various doses. As a result, we observed that BTBR mice have significantly lower plasma sulfate levels and EAAT expression levels in the frontal cortex compared to C57 mice. Surprisingly, neonatal therapeutic dose of APAP administration did not induce behavioral changes in both C57 and BTBR in adolescence. However, we showed that a supratheraputic dose of APAP significantly elevated levels of oxidative stress marker in the brain. Overall, the results suggested that BTBR mice would be a useful mouse model to investigate effects of various environmental factors that have been associated with autism. In addition, early exposure to APAP at supratherapeutic doses may negatively affect normal brain development.
APA, Harvard, Vancouver, ISO, and other styles
7

Schrötter, Sandra. "Specificity of developmental- and growth factor-dependent phosphorylation of Akt isoforms in neurons." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2016. http://dx.doi.org/10.18452/17593.

Full text
Abstract:
Ein Signalweg während der neuronalen Entwicklung im adulten Gehirn ist der PI3K-PTEN-Akt Signalweg. Akt ist eine Kinase die drei verschiedene Isoformen besitzt, welche durch die Phosphorylierung von S473 und T308 aktiviert werden. KO Modelle der Isoformen haben gezeigt, dass nicht alle Funktionen von anderen Isoformen kompensiert werden können. Die genaue Rolle der einzelnen Isoformen in einem neuronalen Zusammenhang ist nur wenig untersucht. Ziel dieser Arbeit war, eine detaillierte Analyse der einzelnen Akt Isoformen nach der Aktivierung des PI3K-PTEN Signalweges. Dazu wurde im Labor eine neue Methode zur isoelektrischen Fokussierung etabliert., welche Proteine nach ihrer Ladung trennt und somit eine Analyse der Dynamik von Akt Phosphorylierungen in neuronalen Zellen erlaubt. Im Zuge dieser Arbeit konnten wir bisher unerkannte Merkmale der Akt Aktivierung und Phosphorylierung identifizieren. Wir konnten zeigen, dass die S473 und T308 Phosphorylierung in Neuroblastomazellen unabhängig voneinander auftreten kann und, dass verschiedene Akt1 Moleküle unterschiedlich auf die Inhibition von PI3K reagieren. Außerdem konnten wir Verschiebungen in der Aktivierung und in der Expression der unterschiedlichen Isoformen während der postnatalen Gehirnentwicklung der Ratte feststellen. Des Weiteren konnten wir zeigen, dass die Aktivierung von Akt von dem Signal und dem Alter der Neurone abhängig ist. Noch nicht vollständig differenzierte Neurone reagieren vor allem auf BDNF Stimulation, wohingegen adulte, differenzierte Neurone hauptsächlich auf EGF reagieren und dort explizit Akt2 über EGFR und PI3K-p110α Signale aktiviert wird. Im Gegensatz dazu führt der Verlust von PTEN zu einer Aktivierung von hauptsächlich Akt1. Zusammenfassend zeigt diese Arbeit einen komplexen Zusammenhang der Phosphorylierung von Akt auf, welcher Signal- und Entwicklungsabhängig ist bei dem unterschiedliche Akt Populationen auf Wachstumsfaktoren und auf PTEN Verlust reagieren.
A major pathway involved in neuronal development is the PI3K-PTEN-Akt pathway. Akt comprises three isoforms, which are activated by phosphorylation of the residues S473 and T308. KO animals for the isoforms have shown differential as well as redundant functions of the three isoforms. However, their individual role in neuronal signaling pathways has not yet been studied in great detail. The aim of this study was to obtain further insight into differential Akt isoform signaling in response to changes in the activity of PI3K and PTEN pathway. A new isoelectric focusing method was established, which allowed us to separate Akt proteins according to their charge, therefore, providing a refined read-out to study dynamics of Akt phosphorylation in a neuronal background. In the course of this project we were able to identify previously undescribed features of Akt phosphorylation and activation. First, we could provide evidence for an uncoupling of the two activating phosphorylation events at S473 and T308 in neuroblastoma cells and differential sensitivities of Akt1 forms towards PI3K inhibition. Secondly, we found a transient shift in Akt isoform activation and abundance during postnatal rat brain development. Thirdly, we were able to show that the activation of different Akt isoforms is dependent of the upstream signal as well as the age of the neuron. Immature neurons were found to be highly responsive to BDNF treatment, whereas mature neurons were most responsive to EGF stimulation leading exclusively to activation of Akt2 in an EGFR- and PI3K/p110α-dependent manner. Stimulation of Akt phosphorylation by the loss of PTEN led to an activation of mainly Akt1 forms, which suggests inherent differences in the Akt pools that are accessible to growth factors dependent PI3Ks as compared to the pools that are controlled by PTEN. In summary, this thesis demonstrates the presence of complex phosphorylation events of Akt in a developmental- and signal-dependent manner in neurons.
APA, Harvard, Vancouver, ISO, and other styles
8

Moore, Daniel. "Novel Role of MeCP2 in Developing Oligodendrocytes and Myelination." VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/2516.

Full text
Abstract:
Methyl-CpG-binding protein 2 (MeCP2 is) is an epigenetic regulator that binds to methylated DNA. Initially identified as transcriptional repressor, MeCP2 also binds to different proteins functioning as gene activator. Importantly, MecCP2 gene mutations and changes in MeCP2 levels are associated to several forms of mental retardation and autism-related disorders; including Rett, a neurodevelopmental disorder affecting primarily girls. While brain MeCP2 was considered to be exclusively neuronal, this regulator is also present in glia. We found that oligodendrocytes, the myelinating cells of the central nervous system (CNS), express particularly high MeCP2 levels at a developmental stage that precedes their final maturation. Moreover, downregulation of MeCP2 levels by treatment of immature oligodendrocytes with small interference RNA (siRNA), reduced the expression of 14 kDa myelin basic protein (MBP) and MOG, two markers of mature oligodendrocytes. These observations raise the possibility that oligodendrocytes have a direct participation in Rett syndrome and other autism-related disorders.
APA, Harvard, Vancouver, ISO, and other styles
9

Dishaw, Laura Victoria. "Halogenated Organophosphate Flame Retardants: Developmental Toxicity and Endocrine Disruptive Effects." Diss., 2015. http://hdl.handle.net/10161/9838.

Full text
Abstract:

Following the phase out of polybrominated diphenyl ethers (PBDEs), manufacturers turned to several alternative flame retardants (FRs) to meet flammability standards. Organophosphate FRs (OPFRs), and in particular tris (1,3-dichloropropyl) phosphate (TDCPP), have been increasingly detected in textiles and foam padding used in a variety of consumer products including camping equipment, upholstered furniture, and baby products. Like PBDEs, OPFRs are additive, meaning that they are not chemically bound to the treated material and can more readily leach out into the surrounding environment. Indeed, OPFRs have been detected in numerous environmental and biological matrices, often at concentrations similar to or exceeding that of PBDEs.

Although OPFRs have been in use for several decades, relatively little is known regarding their potential for adverse human and environmental health consequences. However, based on their structural similarity to OP pesticides, they may have analogous mechanisms of toxicity. OP pesticide toxicity is classically associated with cholinesterase inhibition, resulting in cholinergic intoxication syndrome. OPFRs have been shown to be ineffective cholinesterase inhibitors, however chlorpyrifos (CPF) and other OP pesticides have been shown to elicit adverse effects on developing organisms through other mechanisms.

The main objective of this research project was to evaluate the toxicity of four structurally similar OPFRs (TDCPP; tris (2,3-dibromopropyl) phosphate, (TDBPP); tris (1-chloropropyl) phosphate (TCPP) and tris (2-chloroethyl) phosphate (TCEP)) in comparison to chlorpyrifos (CPF), a well-studied OP pesticide. A combination of in vitro and in vivo models was used to elucidate potential mechanisms as well as functional consequences of exposure in developing organisms.

In the first research aim, a series of in vitro experiments with neurotypic PC12 cells was used to evaluate the effects of four structurally similar OPFRs (TDCPP, TDBPP, TCEP, or TCPP) and CPF on neurodevelopment. The effects of TDCPP were also compared to that of BDE-47, a major component of the commercial PentaBDE mixture. In general, TDCPP elicited similar or greater effects when compared to an equimolar concentration of CPF. All OPFRs tested produced similar decrements in cell number and altered phenotypic differentiation, while BDE-47 had no effect on cell number, cell growth, or neurite growth.

For the second research aim, zebrafish (Danio rerio) were used to evaluate the effects of the same suite of chemicals on early development. TDCPP, TDBPP, and CPF elicited overt toxicity (e.g., malformations or death) within the concentration range tested (0.033-100 µM). TDBPP was the most potent with 100% mortality by 6 days post fertilization (dpf) at ≥3.3 µM. CPF and TDCPP showed equivalent toxicity with malformations observed in at 10 µM and significant mortality (≥75%) at ≥33 µM. There was no overt toxicity among TCEP- and TCPP-exposed fish. All test chemicals affected larval swimming behavior on 6 dpf at concentrations below the overt toxicity threshold. Parent chemical was detected in all in embryonic (1 dpf) and larval (5 dpf) tissues. TDCPP and TDBPP showed rapid and extensive metabolism.

Finally, for the third aim, juvenile (45-55 dpf) zebrafish were exposed to CPF (1 µg/g food) or TDCPP (Low TDCPP = 1 µg/g food; High TDCPP = 40 µg/g food) via diet for 28 days followed by a 7 day depuration period where all treatments received clean food. A dietary exposure was chosen to more closely recapitulate exposure in humans. Samples were collected at seven time points throughout the experiment: days 0, 7, 14, 21, 28, 30, 35. Whole tissues were collected for tissue accumulation and histopathology endpoints. Viscera and brain were dissected and flash frozen separately for DNA damage analyses.

Tissue measurements of CPF, TDCPP, and the metabolite bis (1,3-dichloropropyl) phosphate (BDCPP) were often below the method detection limit, however when present there was a trend towards increased accumulation with treatment and time. On Day 7 Low TDCPP caused a dramatic but transient increase in DNA damage in both viscera and brain that returned to control levels by Day 14. Similar results have been seen previously with other genotoxicants and may be due to CPF and High TDCPP inducing an adaptive response prior to the 7 day sampling point. All treatments shifted the neurohypophysis to adenohypophysis ratio (NH/AH; Day 7 only) and significantly increased thyroid follicle activation (Day 14). Finally High TDCPP affected gonad maturation, causing a significant increase in ovary follicle development (Day 14) and a transient but marked decrease in testes maturity (Day 7). Taken together these data suggest that dietary exposure to TDCPP and CPF elicits DNA damage in brain and viscera and alters endocrine function in juvenile zebrafish. Importantly, analyses were restricted to the first three time points (Days 0, 7, and 14) due to the emergence a disease among the experimental colony. Although these samples were collected prior to the disease becoming apparent, it remains a potential confounder of the current results.


Dissertation
APA, Harvard, Vancouver, ISO, and other styles
10

Choi, Yeyoon. "The role of AF1q in neural development." Thesis, 2019. https://hdl.handle.net/2144/36161.

Full text
Abstract:
ALL1-fused gene from chromosome 1q (AF1q) is a novel gene that encodes a 90-amino-acid protein that is unlike any other known proteins. AF1q was first discovered as a fusion partner for mixed-lineage leukemia in a pediatric acute myeloid leukemia. Since its discovery, AF1q has been found to act as an oncogene and has been linked to several solid neoplasms, including thyroid oncocytic tumors, breast cancer, testicular cancer, and colorectal cancer. AF1q is also upregulated in several hematological malignancies and is considered an adverse prognostic factor. In addition, AF1q is expressed in various regions of the brain throughout human neural developmental processes. The expression levels of AF1q and neuron-specific class III β-tubulin (Tuj1), a marker of post-mitotic neurons, are positively correlated in the cerebral cortex. AF1q expression also induces the transformation of human embryonic kidney cells into neurons, indicating that AF1q may play a key role in neuronal differentiation during normal neural development. The activity of AF1q is regulated by RE1-silencing transcription factor (REST), an important regulator of embryonic and neural stem cells during normal development. Furthermore, AF1q is associated with the activity of the Wingless/Integrated (Wnt) signaling pathway, which is critical to normal development of the nervous system. Although the precise role of AF1q is yet to be uncovered, various studies have demonstrated that AF1q is indeed heavily involved in neurodevelopmental processes. The investigation of the role of AF1q in neurodevelopment is important for several reasons. First, it can give a better understanding of the biological and physiological functions of AF1q, a gene that is still poorly understood. Second, it can provide insight into the development of the human nervous system and the complex processes and regulations that are involved. Through the study of AF1q in a neurobiological context, its precise role in neural development may be uncovered, and new therapeutic approaches to neurodevelopmental disorders such as Down syndrome and Alzheimer’s disease may be possible.
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Developmental biology/neurodevelopment"

1

Eyre, Janet. Neurodevelopmental disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0189.

Full text
Abstract:
Remarkable advances in the neurosciences, particularly in the fields of genetics, molecular biology, metabolism, and nutrition, have greatly advanced our understanding of how the brain develops and responds to environmental influences. Neurodevelopmental disorders arise from perturbation of these normal developmental processes, by insults from heterogeneous aetiological factors. These factors trigger a sequence of molecular, biochemical, and morphological alterations of the brain, resulting in a morphologically and/ or functionally abnormal brain. Rapidly advancing understanding of basic neurodevelopmental processes has direct relevance to understanding human neurodevelopmental disorders, providing insights into pathogenic mechanisms and revealing new pathways that can be exploited in diagnosis and treatment. Conversely the identification of the molecular bases of several neurodevelopmental disorders has also provided invaluable insights into the mechanisms of normal brain development. Technical advances have also improved methods for identifying brain regions involved in developmental disorders, for tracing connections between parts of the brain, for visualizing individual neurons in living brain preparations, for recording the activities of neurons, and for studying the activity of single-ion channels and the receptors for various neurotransmitters. During the past 10 years the genetic basis of an ever increasing number of neurodevelopmental disorders has been discovered and has led to better understanding of the neurobiological basis of even common disorders such as global developmental delay, cerebral palsy, and autism. Current research should reveal their underlying molecular biology and eventually the possibility of targeted chemotherapy and the prevention of many neurodevelopmental disorders.
APA, Harvard, Vancouver, ISO, and other styles
2

Alloway, Tracy Packiam, and Susan E. Gathercole. Working Memory and Neurodevelopmental Disorders. Taylor & Francis Group, 2015.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Alloway, Tracy Packiam, and Susan E. Gathercole. Working Memory and Neurodevelopmental Disorders. Taylor & Francis Group, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Alloway, Tracy Packiam, and Susan E. Gathercole. Working Memory and Neurodevelopmental Disorders. Taylor & Francis Group, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Alloway, Tracy Packiam, and Susan E. Gathercole. Working Memory and Neurodevelopmental Disorders. Taylor & Francis Group, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Alloway, Tracy Packiam, and Susan E. Gathercole. Working Memory and Neurodevelopmental Disorders. Taylor & Francis Group, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Working Memory and Neurodevelopmental Disorders. Psychology Press, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

(Editor), Claudia Maria Vargas, and Patricia Ann Prelock (Editor), eds. Caring for Children With Neurodevelopmental Disabilities and Their Families: An Innovative Approach to Interdisciplinary Practice. Lawrence Erlbaum, 2004.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Prelock, Patricia Ann, and Claudia Maria Vargas. Caring for Children with Neurodevelopmental Disabilities and Their Families: An Innovative Approach to Interdisciplinary Practice. Taylor & Francis Group, 2004.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Prelock, Patricia Ann, and Claudia Maria Vargas. Caring for Children with Neurodevelopmental Disabilities and Their Families: An Innovative Approach to Interdisciplinary Practice. Taylor & Francis Group, 2004.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Developmental biology/neurodevelopment"

1

Crespi, Bernard, and Emma Leach. "The Evolutionary Biology of Human Neurodevelopment." In Developmental Approaches to Human Evolution, 205–30. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118524756.ch9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Neuwirth, Lorenz S., Bright U. Emenike, Eddy D. Barrera, Nimra Hameed, Samantha Rubi, Teddy F. Dacius, Jourvonn C. Skeen, et al. "Assessing the Anxiolytic Properties of Taurine-Derived Compounds in Rats Following Developmental Lead Exposure: A Neurodevelopmental and Behavioral Pharmacological Pilot Study." In Advances in Experimental Medicine and Biology, 801–19. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8023-5_69.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Pappas, Samuel S., Daniel K. Leventhal, Roger L. Albin, and William T. Dauer. "Mouse Models of Neurodevelopmental Disease of the Basal Ganglia and Associated Circuits." In Current Topics in Developmental Biology, 97–169. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-397920-9.00001-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Vohr, Betty R. "Prematurity: Impact on Neurodevelopmental and Behavioral Outcomes." In Cognitive and Behavioral Abnormalities of Pediatric Diseases. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780195342680.003.0050.

Full text
Abstract:
Prematurity continues to be a major public health problem and, despite advances in antenatal care, prematurity rates continue to rise in the United States. Preterm and low-birth-weight (LBW) rates increased in 2006 to 12.8% and 8.3%, respectively. The very low birth weight (VLBW) (<1500 g) rate rose to 1.46% (62,283 of 4,265,996 births in 2006). In addition, the birth rate for women aged 40–44 years rose 3% to 9.4 per 1,000 between 2005 and 2006 (Martin et al. 2008). A component of the increase in the preterm birth rate remains attributed to older maternal childbearing, multiple births, and increasing rates of assisted reproductive technology (Heck et al. 1997). The increase in the number of multiple births is a concern because of the associated increased risk of death, preterm birth, low birth weight, and long-term adverse neurodevelopmental outcomes. Major therapeutic advances in perinatal and neonatal care in the past 20 years, including surfactant therapy, antenatal steroids for both pulmonary maturation and central nervous system protection, improved ventilation techniques, and parenteral nutritional support have resulted in a significant improvement in survival of extremely low-birth-weight infants (ELBW) (<1000 g) (National Institutes of Health [NIH] 1995; El-Metwally, Vohr, and Tucker 2000; Fanaroff, Hack, and Walsh 2003; Fanaroff et al. 2007; Hintz et al. 2005a; Hintz et al. 2005b). These infants have increased complex neonatal medical morbidities affecting all organ systems including lungs, gastrointestinal tract, kidneys, and brain, and increased growth, neurological, developmental, and behavioral morbidities both in the neonatal intensive care unit (NICU) and after discharge (Blakely et al. 2005; Ehrenkranz, 2000; Ehrenkranz et al. 2005; Laptook et al. 2005; Shankaran et al. 2004; Schmidt et al. 2003; Vohr et al. 2003; Vohr et al. 2004;Vohr et al. 2005; Walsh et al. 2005). Predicting the survival and neurodevelopmental outcomes of preterm infants becomes a challenge since outcomes are dependent on a combination of biologic factors including gender, gestational age, birth weight, singleton versus multiple, neonatal morbidities, neonatal interventions, and post-discharge environment.
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Developmental biology/neurodevelopment"

1

Campolo, Domenico, Massimo Molteni, Eugenio Guglielmelli, Flavio Keller, Cecilia Laschi, and Paolo Dario. "Towards Development of Biomechatronic Tools for Early Diagnosis of Neurodevelopmental Disorders." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.260499.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Campolo, Domenico, Massimo Molteni, Eugenio Guglielmelli, Flavio Keller, Cecilia Laschi, and Paolo Dario. "Towards Development of Biomechatronic Tools for Early Diagnosis of Neurodevelopmental Disorders." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4398138.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Developmental biology/neurodevelopment' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography