scholarly journals The Crucial Role of Atg5 in Cortical Neurogenesis During Early Brain Development

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Xiaohui Lv ◽  
Huihui Jiang ◽  
Baoguo Li ◽  
Qingli Liang ◽  
Shukun Wang ◽  
...  
Keyword(s):  
Brain Development ◽  
Crucial Role ◽  
Cortical Neurogenesis ◽  
Early Brain Development

scholarly journals Spatio-Temporal Roles of ASD-Associated Variants in Human Brain Development

Genes ◽  
2020 ◽  
Vol 11 (5) ◽  
pp. 535
Author(s):  
Yujin Kim ◽  
Joon-Yong An
Keyword(s):  
Human Brain ◽  
Brain Development ◽  
De Novo ◽  
Autism Spectrum ◽  
Network Analyses ◽  
Regulatory Variants ◽  
Human Brain Development ◽  
Early Brain Development ◽  
Spatio Temporal

Transcriptional regulation of the genome arguably provides the basis for the anatomical elaboration and dynamic operation of the human brain. It logically follows that genetic variations affecting gene transcription contribute to mental health disorders, including autism spectrum disorder (ASD). A number of recent studies have shown the role of de novo variants (DNVs) in disrupting early neurodevelopment. However, there is limited knowledge concerning the role of inherited variants during the early brain development of ASD. In this study, we investigate the role of rare inherited variations in neurodevelopment. We conducted co-expression network analyses using an anatomically comprehensive atlas of the developing human brain and examined whether rare coding and regulatory variants, identified from our genetic screening of Australian families with ASD, work in different spatio-temporal functions.

scholarly journals Role of thyroid hormone during early brain development

2004 ◽  
pp. U25-U37 ◽  
Author(s):  
G Morreale de Escobar ◽  
MJ Obregon ◽  
F Escobar del Rey
Keyword(s):  
Cerebral Cortex ◽  
Thyroid Hormone ◽  
Brain Development ◽  
Nuclear Receptor ◽  
Biological Significance ◽  
Fetal Brain ◽  
Low T3 ◽  
Early Brain Development ◽  
Fetal Fluids

The present comments are restricted to the role of maternal thyroid hormone on early brain development, and are based mostly on information presently available for the human fetal brain. It emphasizes that maternal hypothyroxinemia - defined as thyroxine (T4) concentrations that are low for the stage of pregnancy - is potentially damaging for neurodevelopment of the fetus throughout pregnancy, but especially so before midgestation, as the mother is then the only source of T4 for the developing brain.Despite a highly efficient uterine-placental 'barrier' to their transfer, very small amounts of T4 and triiodothyronine (T3) of maternal origin are present in the fetal compartment by 4 weeks after conception, with T4 increasing steadily thereafter. A major proportion of T4 in fetal fluids is not protein-bound: the 'free' T4 (FT4) available to fetal tissues is determined by the maternal serum T4, and reaches concentrations known to be of biological significance in adults. Despite very low T3 and 'free' T3 (FT3) in fetal fluids, the T3 generated locally from T4 in the cerebral cortex reaches adult concentrations by midgestation, and is partly bound to its nuclear receptor. Experimental results in the rat strongly support the conclusion that thyroid hormone is already required for normal corticogenesis very early in pregnancy.The first trimester surge of maternal FT4 is proposed as a biologically relevant event controlled by the conceptus to ensure its developing cerebral cortex is provided with the necessary amounts of substrate for the local generation of adequate amounts of T3 for binding to its nuclear receptor. Women unable to increase their production of T4 early in pregnancy would constitute a population at risk for neurological disabilities in their children. As mild-moderate iodine deficiency is still the most widespread cause of maternal hypothyroxinemia in Western societies, the birth of many children with learning disabilities may already be preventable by advising women to take iodine supplements as soon as pregnancy starts, or earlier if possible.

scholarly journals Astrocytes in Down Syndrome Across the Lifespan

2021 ◽  
Vol 15 ◽  
Author(s):  
Blandine Ponroy Bally ◽  
Keith K. Murai
Keyword(s):  
Down Syndrome ◽  
Brain Development ◽  
Chromosome 21 ◽  
Early Brain Development ◽  
The Central Nervous System ◽  
Circuit Development ◽  
And Function ◽  
The Impact ◽  
The Brain

Down Syndrome (DS) is the most common genetic cause of intellectual disability in which delays and impairments in brain development and function lead to neurological and cognitive phenotypes. Traditionally, a neurocentric approach, focusing on neurons and their connectivity, has been applied to understanding the mechanisms involved in DS brain pathophysiology with an emphasis on how triplication of chromosome 21 leads to alterations in neuronal survival and homeostasis, synaptogenesis, brain circuit development, and neurodegeneration. However, recent studies have drawn attention to the role of non-neuronal cells, especially astrocytes, in DS. Astrocytes comprise a large proportion of cells in the central nervous system (CNS) and are critical for brain development, homeostasis, and function. As triplication of chromosome 21 occurs in all cells in DS (with the exception of mosaic DS), a deeper understanding of the impact of trisomy 21 on astrocytes in DS pathophysiology is warranted and will likely be necessary for determining how specific brain alterations and neurological phenotypes emerge and progress in DS. Here, we review the current understanding of the role of astrocytes in DS, and discuss how specific perturbations in this cell type can impact the brain across the lifespan from early brain development to adult stages. Finally, we highlight how targeting, modifying, and/or correcting specific molecular pathways and properties of astrocytes in DS may provide an effective therapeutic direction given the important role of astrocytes in regulating brain development and function.

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