Teratogenetic periods for the principal malformations of the central nervous system

Zamorano, Lucía; Chuaqui, B

doi:10.1007/bf00427147

Cited by 21 publications

(4 citation statements)

References 42 publications

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“…A predilection for the frontal lobe (3/6) might be suggested from the published data and our case, but any cerebral lobe may be affected. When trying to narrow down the timing of the different malformations it is conspicuous that development of corpus callosum, cerebellar vermis, and primary sulci as well as the second cortical migration wave proceeds during the third and fourth months from conception (Zamorano & Chuaqui, 1979). Axial mesodermal defects (i.e., meningocele) may also occur during the same time period early in the fetal period (O'Rahilly & Muller, 1999).…”

Section: Discussionmentioning

confidence: 99%

Sublobar dysplasia—A clinicopathologic report after successful epilepsy surgery

Tuxhorn¹,

Woermann²,

Pannek³

et al. 2009

Epilepsia

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SUMMARYWe report the clinical presentation, neuroradiologic characteristics, and detailed histopathologic findings in a unique case of drug-resistant focal epilepsy due to sublobar dysplasia (SLD), treated successfully by resection of the malformed cortex. Histopathology with leptomeningeal and subcortical heterotopia, disturbance of cortical lamination and marked cortical and subcortical astrocytosis, but absence of balloon cells, points to a disorder of neuronal migration and organization rather than proliferation in SLD. The additional presence of a lateral proboscis and meningocele in our case as well as further associated callosal and cerebellar anomalies may suggest an etiologic unknown damage of pathways controlling the embryogenesis of craniofacial field processes.

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Section: Discussionmentioning

confidence: 99%

Sublobar dysplasia—A clinicopathologic report after successful epilepsy surgery

Tuxhorn¹,

Woermann²,

Pannek³

et al. 2009

Epilepsia

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“…The neural plate eventually gives rise to the entire central nervous sys tem (CNS) and to specialized tissue along its margins that later form the neural crest, from which much of the peripheral nervous system (PNS), including its autonomic com ponents, is derived. Teratogens in this pe riod can have profound effects leading to malformations and embryonal death [5],…”

Section: Neuronal Inductionmentioning

confidence: 99%

Brain Development in the Fetus, Neonate and Infant

Herschkowitz

1988

Neonatology

110

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In structural brain development eight interrelated but distinguishable events can be recognized: (1) neuronal induction, (2) neuroblast proliferation, (3) neuronal migration, (4) neuronal selective aggregation, (5) neuronal differentiation and formation of specific patterns of connection, (6) neuronal death, (7) selective synapse elimination and (8) myelination. The basic mechanisms regulating these developmental events are genetically determined but at any stage of development epigenetic and environmental factors modulate the genetic regulation. This paper reviews representative samples of work in animal experiments and knowledge in human fetal brain development by several authors.

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“…Neural tube closure defects and microcephaly both occur at frequencies of approximately one in 1000 live births (Detrait et al, 2005; Zamorano and Chuaqui, 1979; Krauss et al, 2003). Both genetic and environmental factors contribute to these conditions.…”

Section: Introductionmentioning

confidence: 99%

Development of head organizer of the mouse embryo depends on a high level of mitochondrial metabolism

Zhou¹,

Anderson²

2010

Developmental Biology

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Mouse genetic studies have defined a set of signaling molecules and transcription factors that are necessary to induce the forebrain. Here we describe an ENU-induced mouse mutation, nearly headless (nehe), that was identified based on the specific absence of most of the forebrain at midgestation. Positional cloning and genetic analysis show that, unlike other mouse mutants that disrupt specification of the forebrain, the nehe mutation disrupts mitochondrial metabolism. nehe is a hypomorphic allele of Lipoic acid Synthetase (Lias), the enzyme that catalyzes the synthesis of lipoic acid, an essential cofactor for several mitochondrial multienzyme complexes required for oxidative metabolism. The defect in forebrain development in nehe mutants is apparent as soon as the forebrain is specified, without a concomitant increase in apoptosis. Two tissues required for forebrain specification, the anterior visceral endoderm and the anterior definitive endoderm, develop normally in nehe mutants. However, a third head organizer tissue, the prechordal plate, fails to express markers of cell type determination and shows abnormal morphology in the mutants. We find that the level of phosphorylated (active) AMPK, a cellular energy sensor that affects cell polarity, is up-regulated in nehe mutants at the time when the prechordal plate is normally specified. The results suggest that the nehe phenotype arises because high levels of energy production are required for the specialized morphogenetic movements that generate the prechordal plate, which is required for normal development of the mammalian forebrain. We suggest that a requirement for high levels of ATP for early forebrain patterning may contribute to certain human microcephaly syndromes.

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Teratogenetic periods for the principal malformations of the central nervous system

Cited by 21 publications

References 42 publications

Sublobar dysplasia—A clinicopathologic report after successful epilepsy surgery

Sublobar dysplasia—A clinicopathologic report after successful epilepsy surgery

Brain Development in the Fetus, Neonate and Infant

Development of head organizer of the mouse embryo depends on a high level of mitochondrial metabolism

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