scholarly journals Comparative assessments of the effects of alcohol exposure on fetal brain development using optical coherence tomography and ultrasound imaging

2013 ◽  
Vol 18 (2) ◽  
pp. 020506 ◽  
Author(s):  
Narendran Sudheendran ◽  
Shameena Bake ◽  
Rajesh C. Miranda ◽  
Kirill V. Larin
Keyword(s):  
Optical Coherence Tomography ◽  
Brain Development ◽  
Ultrasound Imaging ◽  
Fetal Brain ◽  
Alcohol Exposure ◽  
Optical Coherence ◽  
Fetal Brain Development

scholarly journals Thiamin deficiency on fetal brain development with and without prenatal alcohol exposure

2018 ◽  
Vol 96 (2) ◽  
pp. 169-177 ◽  
Author(s):  
Olena Kloss ◽  
N.A. Michael Eskin ◽  
Miyoung Suh
Keyword(s):  
Brain Development ◽  
Prenatal Exposure ◽  
Prenatal Alcohol Exposure ◽  
Fetal Brain ◽  
Alcohol Exposure ◽  
Brain Dysfunction ◽  
Negative Effects ◽  
Thiamin Deficiency ◽  
Optimal Health ◽  
Fetal Brain Development

Adequate thiamin levels are crucial for optimal health through maintenance of homeostasis and viability of metabolic enzymes, which require thiamine as a co-factor. Thiamin deficiency occurs during pregnancy when the dietary intake is inadequate or excessive alcohol is consumed. Thiamin deficiency leads to brain dysfunction because thiamin is involved in the synthesis of myelin and neurotransmitters (e.g., acetylcholine, γ-aminobutyric acid, glutamate), and its deficiency increases oxidative stress by decreasing the production of reducing agents. Thiamin deficiency also leads to neural membrane dysfunction, because thiamin is a structural component of mitochondrial and synaptosomal membranes. Similarly, in-utero exposure to alcohol leads to fetal brain dysfunction, resulting in negative effects such as fetal alcohol spectrum disorder (FASD). Thiamin deficiency and prenatal exposure to alcohol could act synergistically to produce negative effects on fetal development; however, this area of research is currently under-studied. This minireview summarizes the evidence for the potential role of thiamin deficiency in fetal brain development, with or without prenatal exposure to alcohol. Such evidence may influence the development of new nutritional strategies for preventing or mitigating the symptoms of FASD.

Effect of alcohol exposure on fetal brain development

2013 ◽  
Author(s):  
Narendran Sudheendran ◽  
Shameena Bake ◽  
Rajesh C. Miranda ◽  
Kirill V. Larin
Keyword(s):  
Brain Development ◽  
Fetal Brain ◽  
Alcohol Exposure ◽  
Fetal Brain Development

New normal range of fetal cavum septum pellucidum in the second trimester of gestation

2020 ◽  
Author(s):  
M.V. Medvedev, O.I. Kozlova, À.Yu. Romanova
Keyword(s):  
Brain Development ◽  
Reference Range ◽  
Fetal Brain ◽  
Septum Pellucidum ◽  
Second Trimester ◽  
Normal Range ◽  
Cavum Septum Pellucidum ◽  
New Normal ◽  
Biparietal Diameter ◽  
Fetal Brain Development

Fetal brain was retrospectively evaluated in 418 normal fetuses at 16–28 weeks of gestation. The multiplanar mode to obtain the axial cerebral plane and measured the width of the cavum septum pellucidum (CSP) and biparietal diameter (BD). All measurements of CSP were done from as the widest diameter across both borders in an inter-to inter fashion. The CSP width is increasing at second trimester of gestation. Normal range plotted on the reference range (mean, 5th and 95th percentiles) of fetal width CSP by measuring of its size may be useful for assessment of fetal brain development in the second trimester of gestation.

scholarly journals CB1 antagonism increases excitatory synaptogenesis in a cortical spheroid model of fetal brain development

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Alexis Papariello ◽  
David Taylor ◽  
Ken Soderstrom ◽  
Karen Litwa
Keyword(s):  
Brain Development ◽  
Spontaneous Activity ◽  
Microelectrode Array ◽  
Cannabinoid Receptor ◽  
Fetal Brain ◽  
Endocannabinoid System ◽  
Autism Spectrum ◽  
Nervous System Development ◽  
Inhibitory Synapses ◽  
Fetal Brain Development

AbstractThe endocannabinoid system (ECS) plays a complex role in the development of neural circuitry during fetal brain development. The cannabinoid receptor type 1 (CB1) controls synaptic strength at both excitatory and inhibitory synapses and thus contributes to the balance of excitatory and inhibitory signaling. Imbalances in the ratio of excitatory to inhibitory synapses have been implicated in various neuropsychiatric disorders associated with dysregulated central nervous system development including autism spectrum disorder, epilepsy, and schizophrenia. The role of CB1 in human brain development has been difficult to study but advances in induced pluripotent stem cell technology have allowed us to model the fetal brain environment. Cortical spheroids resemble the cortex of the dorsal telencephalon during mid-fetal gestation and possess functional synapses, spontaneous activity, an astrocyte population, and pseudo-laminar organization. We first characterized the ECS using STORM microscopy and observed synaptic localization of components similar to that which is observed in the fetal brain. Next, using the CB1-selective antagonist SR141716A, we observed an increase in excitatory, and to a lesser extent, inhibitory synaptogenesis as measured by confocal image analysis. Further, CB1 antagonism increased the variability of spontaneous activity within developing neural networks, as measured by microelectrode array. Overall, we have established that cortical spheroids express ECS components and are thus a useful model for exploring endocannabinoid mediation of childhood neuropsychiatric disease.

scholarly journals Neuroplacentology in congenital heart disease: placental connections to neurodevelopmental outcomes

2021 ◽  
Author(s):  
Rachel L. Leon ◽  
Imran N. Mir ◽  
Christina L. Herrera ◽  
Kavita Sharma ◽  
Catherine Y. Spong ◽  
...  
Keyword(s):  
Brain Development ◽  
Congenital Heart ◽  
Fetal Brain ◽  
In Utero ◽  
Structure And Function ◽  
Brain Growth ◽  
Neurodevelopmental Outcomes ◽  
Fetal Brain Development ◽  
And Function

Abstract Children with congenital heart disease (CHD) are living longer due to effective medical and surgical management. However, the majority have neurodevelopmental delays or disorders. The role of the placenta in fetal brain development is unclear and is the focus of an emerging field known as neuroplacentology. In this review, we summarize neurodevelopmental outcomes in CHD and their brain imaging correlates both in utero and postnatally. We review differences in the structure and function of the placenta in pregnancies complicated by fetal CHD and introduce the concept of a placental inefficiency phenotype that occurs in severe forms of fetal CHD, characterized by a myriad of pathologies. We propose that in CHD placental dysfunction contributes to decreased fetal cerebral oxygen delivery resulting in poor brain growth, brain abnormalities, and impaired neurodevelopment. We conclude the review with key areas for future research in neuroplacentology in the fetal CHD population, including (1) differences in structure and function of the CHD placenta, (2) modifiable and nonmodifiable factors that impact the hemodynamic balance between placental and cerebral circulations, (3) interventions to improve placental function and protect brain development in utero, and (4) the role of genetic and epigenetic influences on the placenta–heart–brain connection. Impact Neuroplacentology seeks to understand placental connections to fetal brain development. In fetuses with CHD, brain growth abnormalities begin in utero. Placental microstructure as well as perfusion and function are abnormal in fetal CHD.

Fetal brain development of twins assessed in utero by ultrasound: implications for schizophrenia

1996 ◽  
Vol 19 (2-3) ◽  
pp. 141-149 ◽  
Author(s):  
John H. Gilmore ◽  
Diana O. Perkins ◽  
Mark A. Kliewer ◽  
Marvin L. Hage ◽  
Susan G. Silva ◽  
...  
Keyword(s):  
Brain Development ◽  
Fetal Brain ◽  
In Utero ◽  
Fetal Brain Development

scholarly journals Neural stem cell erythropoietin receptor expression during human fetal brain development

2008 ◽  
Vol 319 (2) ◽  
pp. 553
Author(s):  
Hsiao-Nan Hao ◽  
Jane Zhao ◽  
Kaveh Barami ◽  
Lawrence Morawa
Keyword(s):  
Stem Cell ◽  
Brain Development ◽  
Neural Stem Cell ◽  
Fetal Brain ◽  
Erythropoietin Receptor ◽  
Receptor Expression ◽  
Human Fetal Brain ◽  
Fetal Brain Development

scholarly journals Using optical coherence tomography to rapidly phenotype and quantify congenital heart defects associated with prenatal alcohol exposure

2015 ◽  
Vol 244 (4) ◽  
pp. 607-618 ◽  
Author(s):  
Ganga Karunamuni ◽  
Shi Gu ◽  
Yong Qiu Doughman ◽  
Amanda I. Noonan ◽  
Andrew M. Rollins ◽  
...  
Keyword(s):  
Optical Coherence Tomography ◽  
Congenital Heart Defects ◽  
Congenital Heart ◽  
Prenatal Alcohol Exposure ◽  
Heart Defects ◽  
Alcohol Exposure ◽  
Optical Coherence ◽  
Prenatal Alcohol

scholarly journals Methylomic trajectories across human fetal brain development

2015 ◽  
Vol 25 (3) ◽  
pp. 338-352 ◽  
Author(s):  
Helen Spiers ◽  
Eilis Hannon ◽  
Leonard C. Schalkwyk ◽  
Rebecca Smith ◽  
Chloe C.Y. Wong ◽  
...  
Keyword(s):  
Brain Development ◽  
Fetal Brain ◽  
Human Fetal Brain ◽  
Fetal Brain Development
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