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Disorders of Keratinization and Other Genodermatoses
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Roselyn Stanger, Nanette Silverberg
Overview: This neuroectodermal disorder affects the skin, hair, teeth, eyes, and central nervous system. The condition results from a mutation of the X-chromosome gene NEMO/IKK -gamma gene, which is located on chromosome Xq28. The X-chromosome is inactivated selectively in girls, such that only one is active in any cell; therefore, there can be mosaic involvement of the skin and tissues. Patients can suffer from seizures, developmental delays, and visual impairment.
Neoplasia
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Many tissues of the body are derived from neuroectoderm – the brain, neurons and supporting glia, peripheral nerves (including axons and their supporting Schwann cells), and melanocytes. Tumours derived from these cells are discussed in detail in the appropriate chapters.
Nervous System
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Mark T. Butt, Alys Bradley, Robert Sills
The neural tube develops as the neuroectoderm proliferates, folds, and fuses, resulting in a central tube (deLahunta and Glass 2009). A column of neural crest cells forms dorsolateral to the developing tube. These neural crest cells give rise to many of the components of the peripheral nervous system, including neurons within the dorsal root, sympathetic and parasympathetic (postganglionic) ganglia, the adrenal medulla, melanoblasts, Schwann cells (deLahunta and Glass 2009), and satellite glial cells (SGC).
Focus on eye care in schizophrenia
Published in Clinical and Experimental Optometry, 2019
Oculomotor and alignment abnormalities can be associated with schizophrenia, as seen with Patient 1 who was noted to have a constant exotropia. A recent study has found a significant association between schizophrenia and congenital constant exotropia, with possible genetic ties to polymorphisms in the PMX2B/PHOX2b gene location.2011 Compared to the relatively low incidence of strabismus in the general population, studies have found up to 13 per cent of patients with schizophrenia exhibited exotropia.2017 In fact, childhood exotropia confers a 3.1 times greater likelihood of developing a psychiatric disorder, including schizophrenia.2008 In general, patients with schizophrenia are known to have a higher prevalence of minor physical anomalies, for example performance task, span of apprehension, verbal declarative memory, total brain volume, neurological soft signs, and schizotypy,2013 which can be traced to abnormal fetal development of the neuroectodermal chain.2004 Despite an incomplete understanding of schizophrenia pathogenesis, this developmental disruption is thought to initiate the neurobiological changes that result in schizophrenia.
Retinal nerve fiber layer, macular thickness and anterior segment measurements in attention deficit and hyperactivity disorder
Published in Psychiatry and Clinical Psychopharmacology, 2019
Embryologically, eye and brain development are parallel to each other. The retina and cerebral cortex originating from the neuroectoderm are part of the central nervous system (CNS). The retina and the brain are connected by the optic nerve and the optic nerve loses myelin before it enters the eye. Retinal nerve fibres are unmyelinated axons of nerve cells and appear to be equivalent to the cerebral cortex [6]. CNS pathologies have ocular manifestations due to degeneration of the visual pathways; so, in neurodegenerative diseases such as Multiple Sclerosis, Parkinson's disease, retinal changes associated with changes in brain tissue have been shown [7–10].
Silver nanoparticles inhibit neural induction in human induced pluripotent stem cells
Published in Nanotoxicology, 2018
Shigeru Yamada, Daiju Yamazaki, Yasunari Kanda
To investigate whether AgNPs affect early neurodevelopment, we examined neural differentiation capability of iPSCs, which was induced by dual SMAD inhibition protocol (Chambers et al. 2009) (Figure 1(A)). First, we determined the critical concentration of AgNPs, affecting neural differentiation. At day 4 after neural induction with different concentrations of AgNPs, the expression of PAX6, a neuroectodermal marker that regulates neurogenesis (Manuel et al. 2015), was analyzed using real-time PCR. It was observed that exposure to 0.1 or 0.3 μg/mL AgNPs significantly decreased PAX6 expression (Figure 1(B)). In the case of exposure at 1 μg/mL, AgNPs caused the intense cell detachment at day 0, and neural differentiation could not be assessed. Since 0.3 μg/mL AgNPs decreased PAX6 more effectively than the other doses, this concentration was used for the subsequent experiments. The previous report indicated that PAX6-positive neuroepithelial layer was observed in the neuroectoderm after neural induction (Chambers et al. 2009). We also observed PAX6-positive neuroepithelial cells in vehicle-treated control at day 4 after neural induction (Figure 1(C)). In contrast, AgNPs partially inhibited the formation of PAX6-positive neuroepithelium. Next, we examined the expression of several neural differentiation markers at days 2, 6, and 8, after exposure to 0.3 μg/mL AgNPs. At day 9, almost all cells exposed to AgNPs (0.3 μg/mL) were detached from culture dishes. Real-time PCR analysis revealed that AgNPs decreased the expression of OTX2 and FOXG1, another neuroectodermal markers that regulate neurogenesis (Mortensen et al. 2015; Shen et al. 2006), by day 2 (Figure 1(D)) and day 6 (Figure 1(E)), respectively. Furthermore, it was observed that by day 8, AgNPs decreased the expression of NPC marker Nestin (Hendrickson et al. 2011) (Figure 1(F)). These data suggest that AgNPs have an inhibitory effect on early neural differentiation of iPSCs.