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Nadia Rachdaoui, Ling Li, Belinda Willard, Takhar Kasumov, Stephen Previs, Dipak Sarkar
BACKGROUND: Alcohol consumption during pregnancy is a significant public health problem and can result in a continuum of adverse outcomes to the fetus known as fetal alcohol spectrum disorders (FASD). Subjects with FASD show significant neurological deficits, ranging from microencephaly, neurobehavioral, and mental health problems to poor social adjustment and stress tolerance. Neurons are particularly sensitive to alcohol exposure. The neurotoxic action of alcohol, i.e., through ROS production, induces DNA damage and neuronal cell death by apoptosis...
2017: Clinical Epigenetics
Maia Delaine, Anne-Sophie Weingertner, Antoine Nougairede, Quentin Lepiller, Samira Fafi-Kremer, Romain Favre, Rémi Charrel
We report congenital microencephaly caused by infection with lymphocytic choriomeningitis virus in the fetus of a 29-year-old pregnant women at 23 weeks' gestation. The diagnosis was made by ultrasonography and negative results for other agents and confirmed by a positive PCR result for lymphocytic choriomeningitis virus in an amniotic fluid sample.
September 2017: Emerging Infectious Diseases
Jørgen S Agerholm, Fintan J McEvoy, Steffen Heegaard, Carole Charlier, Vidhya Jagannathan, Cord Drögemüller
BACKGROUND: Surveillance for bovine genetic diseases in Denmark identified a hitherto unreported congenital syndrome occurring among progeny of a Holstein sire used for artificial breeding. A genetic aetiology due to a dominant inheritance with incomplete penetrance or a mosaic germline mutation was suspected as all recorded cases were progeny of the same sire. Detailed investigations were performed to characterize the syndrome and to reveal its cause. RESULTS: Seven malformed calves were submitted examination...
August 2, 2017: BMC Genetics
Megan C Mladinich, John Schwedes, Erich R Mackow
Zika virus (ZIKV) is a mosquito-borne Flavivirus that has emerged as the cause of encephalitis and fetal microencephaly in the Americas. ZIKV uniquely persists in human bodily fluids for up to 6 months, is sexually transmitted, and traverses the placenta and the blood-brain barrier (BBB) to damage neurons. Cells that support persistent ZIKV replication and mechanisms by which ZIKV establishes persistence remain enigmatic but central to ZIKV entry into protected neuronal compartments. The endothelial cell (EC) lining of capillaries normally constrains transplacental transmission and forms the BBB, which selectively restricts access of blood constituents to neurons...
July 11, 2017: MBio
Bor Luen Tang
Zika virus (ZIKV) infection has been associated with congenital microcephaly and peripheral neuropathy. The ongoing epidemic has triggered swift responses in the scientific community, and a number of recent reports have now confirmed a causal relationship between ZIKV infection and birth defect. In particular, ZIKV has been shown to be capable of compromising and crossing the placental barrier and infect the developing fetal brain, resulting in the demise and functional impairment of neuroprogenitor cells critical for fetal cortex development...
September 2016: Archives of Microbiology
Pablo Martínez de Salazar, Anna Suy, Adrián Sánchez-Montalvá, Carlota Rodó, Fernando Salvador, Israel Molina
Zika fever is an arboviral systemic disease that has recently become a public health challenge of global concern after its spread through the Americas. This review highlights the current understanding on Zika virus epidemiology, its routes of transmission, clinical manifestations, diagnostic tests, and the current management, prevention and control strategies. It also delves the association between Zika infection and complications, such as microencephaly or Guillem-Barré syndrome.
April 2016: Enfermedades Infecciosas y Microbiología Clínica
Clare J Wilhelm, Marina Guizzetti
Alcohol consumption during pregnancy can produce a variety of central nervous system (CNS) abnormalities in the offspring resulting in a broad spectrum of cognitive and behavioral impairments that constitute the most severe and long-lasting effects observed in fetal alcohol spectrum disorders (FASD). Alcohol-induced abnormalities in glial cells have been suspected of contributing to the adverse effects of alcohol on the developing brain for several years, although much research still needs to be done to causally link the effects of alcohol on specific brain structures and behavior to alterations in glial cell development and function...
2015: Frontiers in Integrative Neuroscience
Amanjot Kaur Riar, Madhusudhanan Narasimhan, Mary Latha Rathinam, George I Henderson, Lenin Mahimainathan
BACKGROUND: Developing brain is a major target for alcohol's actions and neurological/functional abnormalities include microencephaly, reduced frontal cortex, mental retardation and attention-deficits. Previous studies have shown that ethanol altered the lateral ventricular neuroepithelial cell proliferation. However, the effect of ethanol on subventricular basal progenitors which generate majority of the cortical layers is not known. METHODS: We utilized spontaneously immortalized rat brain neuroblasts obtained from cultures of 18-day-old fetal rat cerebral cortices using in vitro ethanol exposures and an in utero binge model...
January 19, 2016: Journal of Biomedical Science
Diana Le Duc, Ana Spataru, Mihai Ceanga, Leon Zagrean, Torsten Schöneberg, Emil C Toescu, Ana-Maria Zagrean
Prenatal alcohol exposure is associated with microencephaly, cognitive and behavioral deficits, and growth retardation. Some of the mechanisms of ethanol-induced injury, such as high level oxidative stress and overexpression of pro-apoptotic genes, can increase the sensitivity of fetal neurons towards hypoxic/ischemic stress associated with normal labor. Thus, alcohol-induced sequelae may be the cumulative result of direct ethanol toxicity and increased neuronal vulnerability towards metabolic stressors, including hypoxia...
July 21, 2015: Brain Research
Jason Howitt, Ley-Hian Low, Ulrich Putz, Anh Doan, Jenny Lackovic, Choo-Peng Goh, Jenny Gunnersen, John Silke, Seong-Seng Tan
Pten controls a signaling axis that is implicated to regulate cell proliferation, growth, survival, migration, and metabolism. The molecular mechanisms underlying the specificity of Pten responses to such diverse cellular functions are currently poorly understood. Here we report the control of Pten activity and signaling specificity during the cell cycle by Ndfip1 regulation of Pten spatial distribution. Genetic deletion of Ndfip1 resulted in a loss of Pten nuclear compartmentalization and increased cell proliferation, despite cytoplasmic Pten remaining active in regulating PI3K/Akt signaling...
April 2015: Journal of Molecular Cell Biology
Bahri Karacay, Jo Mahoney, Jeffrey Plume, Daniel J Bonthius
BACKGROUND: Prenatal alcohol exposure can kill developing neurons, leading to microencephaly and mental retardation. However, not all fetuses are equally vulnerable to alcohol's neurotoxic effects. While some fetuses are severely affected and are ultimately diagnosed with fetal alcohol syndrome (FAS), others have no evidence of neuropathology and are behaviorally normal. These widely different outcomes among alcohol-exposed fetuses are likely due, in part, to genetic differences. Some fetuses possess genotypes that make them much more vulnerable than others to alcohol's teratogenic effects...
February 2015: Alcoholism, Clinical and Experimental Research
Daniel J Bonthius, Zachary Winters, Bahri Karacay, Samantha Larimer Bousquet, Daniel J Bonthius
The cerebellum is a major target of alcohol-induced damage in the developing brain. However, the cerebella of some children are much more seriously affected than others by prenatal alcohol exposure. As a consequence of in utero alcohol exposure, some children have substantial reductions in cerebellar volume and corresponding neurodevelopmental problems, including microencephaly, ataxia, and balance deficits, while other children who were exposed to similar alcohol quantities are spared. One factor that likely plays a key role in determining the impact of alcohol on the fetal cerebellum is genetics...
January 2015: Neurotoxicology
Yumi Okoshi, Masaharu Hayashi, Sachiko Kanda, Toshiyuki Yamamoto
We reported a 64-year-old autopsy case, showing a unique combination of disorders in visceral organs and brain. She had developmental delay, microencephaly, and facial dysmorphism. She developed sick sinus syndrome and liver cirrhosis. There were no abnormalities in laboratory tests for congenital metabolic errors or anomaly syndromes, including activities of lysosomal enzymes, isoelectric focusing of serum transferrin or array comparative genomic hybridization. She died of cardiorespiratory failure. At autopsy she showed liver cirrhosis and mesangial proliferation...
September 2014: Brain & Development
Joseph D Tingling, Shameena Bake, Rhonda Holgate, Jeremy Rawlings, Phillips P Nagsuk, Jayashree Chandrasekharan, Sarah L Schneider, Rajesh C Miranda
BACKGROUND: Ethanol is a potent teratogen. Its adverse neural effects are partly mediated by disrupting fetal neurogenesis. The teratogenic process is poorly understood, and vulnerable neurogenic stages have not been identified. Identifying these is a prerequisite for therapeutic interventions to mitigate effects of teratogen exposures. METHODS: We used flow cytometry and qRT-PCR to screen fetal mouse-derived neurosphere cultures for ethanol-sensitive neural stem cell (NSC) subpopulations, to study NSC renewal and differentiation...
2013: PloS One
Azam Ramezani, Iran Goudarzi, Taghi Lashkarboluki, Mohammad Taghi Ghorbanian, Kataneh Abrari, Mahmoudi Elahdadi Salmani
OBJECTIVE(S): The purpose of this study was to investigate the role of oxidative stress in Purkinje cell neurotoxicity of ethanol-treated rat. MATERIALS AND METHODS: Male rat pups 4-day-old was used in this study. Ethanol was administered to rat pups at a dose of 6 g/kg from postnatal days (PDs) 4 to 5. Pups were killed 90 min after the second alcohol treatment on PD 5 by decapitation and the brain was immediately removed. The cerebellum was dissected for analyzing the oxidative stress parameters and histological study...
July 2012: Iranian Journal of Basic Medical Sciences
Daniel J Bonthius
Lymphocytic choriomeningitis virus (LCMV) is an important cause of neurologic disease in humans. Carried and secreted principally by wild mice, LCMV covers a large geographic range and infects great numbers of people. Humans acquire LCMV disease when they come into contact with the secretions of infected mice. Because it has a strong neurotropism, the clinical signs and symptoms of LCMV infection are mostly neurologic. When the virus is acquired postnatally by children or adults, the clinical manifestations are usually those of aseptic meningitis...
September 2012: Seminars in Pediatric Neurology
A P Milovanov, O A Milovanova
For the first time in pediatric pathologicoanatomic practice the complete systematization of cerebral cortex malformations is represented. Organ, macroscopic forms: microencephaly, macroencephaly, micropolygyria, pachygyria, schizencephaly, porencephaly, lissencephaly. Histic microdysgenesis of cortex: type I includes isolated abnormalities such as radial (IA) and tangential (I B) subtypes of cortical dislamination; type II includes sublocal cortical dislamination with immature dysmorphic neurons (II A) and balloon cells (II B); type III are the combination focal cortical dysplasia with tuberous sclerosis of the hippocampus (III A), tumors (III B) and malformations of vessels, traumatic and hypoxic disorders (III C)...
September 2011: Arkhiv Patologii
Annika Herrmann, W Hecht, C Herden
No abstract text is available yet for this article.
2011: Tierärztliche Praxis. Ausgabe K, Kleintiere/Heimtiere
C Xiang, V Baubet, S Pal, L Holderbaum, V Tatard, P Jiang, R V Davuluri, N Dahmane
Although neurogenic pathways have been described in the developing neocortex, less is known about mechanisms ensuring correct neuronal differentiation thus also preventing tumor growth. We have shown that RP58 (aka zfp238 or znf238) is highly expressed in differentiating neurons, that its expression is lost or diminished in brain tumors, and that its reintroduction blocks their proliferation. Mice with loss of RP58 die at birth with neocortical defects. Using a novel conditional RP58 allele here we show that its CNS-specific loss yields a novel postnatal phenotype: microencephaly, agenesis of the corpus callosum and cerebellar hypoplasia that resembles the chr1qter deletion microcephaly syndrome in human...
April 2012: Cell Death and Differentiation
Brendan Fitzgerald, Mark O'Driscoll, Karen Chong, Sarah Keating, Patrick Shannon
Seckel syndrome is a rare autosomal recessive disorder characterized by intrauterine growth retardation, dwarfism, microcephaly and mental retardation. Pathological descriptions of fetal stage Seckel syndrome are rare and pre-date the evolving understanding of the genetic and molecular mechanisms involved. The autopsy findings in a case of fetal Seckel syndrome at 30 weeks gestation are presented, with detailed description of the neuropathological findings. Severe neurological abnormalities in a male fetus were observed that included microencephaly, cortical neuronal migration disorder, white matter tract hypoplasia/aplasia, premature depletion of the germinal matrix with cystic transformation and patchy absence of the external granular cell layer of the cerebellum...
March 2012: Brain & Development
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