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Insulin/IGF Signaling in Early Brain Development
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Selma Yagoub, Rachel N. Lippert
In the initial phases of nervous system development in humans and in animals, the developing neural tube undergoes closure during a process called neurulation (8). During this phase, elevated proinsulin, insulin, or blockade of insulin receptor (InsR) signaling either promote cell survival or increase apoptotic events, respectively (9). The most commonly used model to study neurulation has historically been the chick embryo which only has a single preproinsulin gene similar to humans, whereas rodents express two preproinsulin genes (10). This developmental step precedes the formation of the pancreas; however, preproinsulin expression is found in early neurulation in Xenopus laevis (11). The source of this preproinsulin is in part due to the activity of promoting factors, such as Insulin-promoting-factor-1, Ipf1 whose expression and activity precede the formation of the pancreas but supports early detection of insulin in the dorsal foregut endoderm at the 20 somite stage in rodents (12–14). However, other studies show that neuronal subpopulations may also be able to produce and secrete insulin either via detection in subregions of the brain using in situ hybridization (15) or through primary neuronal cultures at various time points in early development (16, 17).
Developmental Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James H. Tonsgard, Nikolas Mata-Machado
Defects in folding, fusion, or closure of the neural tube occur between days 20 and 29 of gestation. Defects involve a variable portion of the dorsal midline structures of the primitive neural tube including its covering of meninges, bone, and skin. Defects can occur anywhere along the neural axis. Defects can also result in the formation of the notochord and secondary neurulation. Both genetic and environmental factors are known to play a role in NTDs. NTDs are associated with a number of genetic syndromes and chromosomal abnormalities, but no one single gene has been implicated as a causative agent.
Tethered Cord Syndrome
Published in Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg, Essentials of the Adult Neurogenic Bladder, 2020
Nishant Garg, Yahir Santiago-Lastra
The central nervous system is formed through three major processes over the first 2 months postconception, with the most critical portion for TCS occurring during the first 2–4 weeks and then during weeks 9–11.7 These stages are broken down into the following: neurulation (neural tube formation), canalization of the tail bud, and regression.8 Neurulation results in folding of the neural plate on itself to form the neural tube. Any errors during this process are likely to result in disorders associated with TCS such as LMMCs, MMCs, and other spinal dysraphisms. The second major process, canalization of the tail bud, occurs when the caudal cell mass is stimulated through an unknown mechanism to undergo canalization and eventual regression.9 This process continues until the only remaining components are the medulla spinalis below T12 and a distal filum terminale, and any anomalies in this process are thought to result in the increased risk and eventual development of TCS.
Eye Abnormalities in Children with Fetal Alcohol Spectrum Disorders: A Systematic Review
Published in Ophthalmic Epidemiology, 2023
Tracey W Tsang, Amy Finlay-Jones, Kerrin Perry, John R Grigg, Svetlana Popova, Melissa Mei Yin Cheung, Carol Bower, Patrick Tam, Robyn V Jamieson, Elizabeth J Elliott
Our findings are biologically plausible. Fetal eye development begins at about three weeks gestation and is dependent on the Sonic Hedgehog gene (Shh), paired box gene 6 (PAX6), and retinoic acid. A period of rapid growth is observed between eight- and 14-weeks’ gestation, during which time the contents of the globe (e.g., the retina and lens) start to develop, before development slows after 30 weeks.63,64 PAE causes a down-regulation of the Shh gene, resulting in disruption of the development and migration of neural crest cells during gastrulation and neurulation, and producing the characteristic midface abnormalities seen in FAS.65,66 The initiation and progression of fetal eye development is dependent on PAX6 and retinoic acid.63,64,67 Ethanol affects PAX6 gene expression by disrupting Shh activity (which regulates PAX6), resulting in abnormalities in eye development.63,68 Ethanol also reduces the retinal conversion of vitamin A (retinol) into retinoic acid,69 which is implicated in the formation of the optic vesicle and cup, lens pit, retina, and anterior segment.67,70 Disruption of the retinoic acid signalling pathway may result in ocular abnormalities including microphthalmos, coloboma, and anophthalmia.70
Selenium and L-carnitine protects from valproic acid-Induced oxidative stress and mitochondrial damages in rat cortical neurons
Published in Drug and Chemical Toxicology, 2022
Ahmad Salimi, Nasrin Alyan, Nasim Akbari, Zhaleh Jamali, Jalal Pourahmad
Oxidative stress has been implicated in the mechanisms of cytotoxicity and teratogenesis of VPA (Chateauvieux et al. 2010). The well-known fetal valproate syndrome, spina bifida is a neural tube defect (NTD) that results from failure of the caudal neural tube to close during organogenesis after exposure with VPA. The brain and the spinal cord develop from the neural tube through the process of neurulation during organogenesis (Tung and Winn 2011). In the current study, we chose the neonatal rats for isolation of neurons due to previous studies have been suggested that young children (less than 7.5 years) have an increased risk of toxicity of valproic acid (Star et al. 2014). Our results showed that valproic acid is toxic for isolated rat neurons up to 50 µM. Previous studies have shown that the therapeutic and toxic concentrations range for valproic acid is 40–100 and 100–200 mg/L respectively (Schulz et al. 2012). Therefore, used concentrations in this study are in therapeutic and toxic range of valproic acid (Figure 1). Interestingly, some studies have been shown neuroprotective effect of valproic acid, therefore this has a controversial effect with our results (Ximenes et al. 2015, Silva et al. 2018). However, the mentioned effect as protective have been shown in adult animals and neurodegenerative disease models, while our results obtained from in vitro models in isolated neurons.
Congenital Spinal Lipomatous Malformations. Part 1. Spinal Lipomas, Lipomyeloceles, and Lipomyelomeningoceles
Published in Fetal and Pediatric Pathology, 2020
Surgical classifications of lumbosacrococcygeal malformations are based on surgical anatomy and embryologic evidence. These studies often suggest that open neural tube defects (e.g., myelomeningoceles) form rostral to the junction of the two neural tubes while congenital spinal lipomatous malformations begin in the embryo caudal to this point from defective secondary neurulation. However, some of the clinical discussion describes some congenital spinal lipomatous malformations as originating from the primary neural tube while others arise from secondary neurulation or from both [1, 17, 28, 31, 40, 120, 164]. It is also acknowledged that congenital spinal lipomatous malformations are being treated for clinical indications without a clear elucidation of their embryologic origin [73, 120].