scholarly journals Cranial index of children with normal and abnormal brain development in Sokoto, Nigeria: A comparative study

2014 ◽  
Vol 5 (02) ◽  
pp. 139-143 ◽  
Author(s):  
Muhammad Awwal Musa ◽  
Abdullahi Daudu Zagga ◽  
Mohammed Danfulani ◽  
Aziz Abdo Tadros ◽  
Ahmed Hamid
Keyword(s):  
Comparative Study ◽  
Brain Development ◽  
Neurodevelopmental Disorders ◽  
Neurodevelopmental Disorder ◽  
Head Length ◽  
Head Width ◽  
Normal Brain ◽  
Anatomical Landmarks ◽  
Cranial Index ◽  
Abnormal Brain

ABSTRACT Background: Abnormal brain development due to neurodevelopmental disorders in children has always been an important concern, but yet has to be considered as a significant public health problem, especially in the low- and middle-income countries including Nigeria. Aims: The aim of this study is to determine whether abnormal brain development in the form of neurodevelopmental disorders causes any deviation in the cranial index of affected children. Materials and Methods: This is a comparative study on the head length, head width, and cranial index of 112 children (72 males and 40 females) diagnosed with at least one abnormal problem in brain development, in the form of a neurodevelopmental disorder (NDD), in comparison with that of 218 normal growing children without any form of NDD (121 males and 97 females), aged 0-18 years old seen at the Usmanu Danfodiyo University Teaching Hospital, Sokoto, over a period of six months, June to December, 2012. The head length and head width of the children was measured using standard anatomical landmarks and cranial index calculated. The data obtained was entered into the Microsoft excel worksheet and analyzed using SPSS version 17. Results: The mean Cephalic Index for normal growing children with normal brain development was 79.82 ± 3.35 and that of the children with abnormal brain development was 77.78 ± 2.95 and the difference between the two groups was not statistically significant (P < 0.05). Conclusion: It can be deduced from this present study that the cranial index does not change in children with neurodevelopmental disorders.

scholarly journals Head shape determination and cranial evaluation using anatomical landmarks in children with sickle cell disease (SCD)

2014 ◽  
Vol 6 (1) ◽  
pp. 98-102 ◽  
Author(s):  
MA Musa ◽  
AD Zagga ◽  
K Musa ◽  
M Danfulani ◽  
H Ahmed
Keyword(s):  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Head Circumference ◽  
Head Length ◽  
Sub Saharan Africa ◽  
Head Width ◽  
Anatomical Landmarks ◽  
Cell Disease ◽  
Cranial Index ◽  
The Mean

Background: Sickle cell disease is one of the commonest diseases widespread in sub-Saharan Africa and Nigeria in particular. This study investigated the possible effects of sickle cell disease (SCD) on the cranial index and pattern of head shapes of children with sickle cell disease in comparison with that of children without SCD. Methods: The head length, head width of 103 children (54 males and 49 females) with sickle cell disease and 218 normal growing non-sickle cell disease children (121 males and 97 females) aged 0-18 years old were measured and their cranial indices calculated. Results: The mean CI for normal growing non sickle cell disease children was 79.82±3.35 and that of the sickle cell disease children was 80.12±3.39 which was not statistically signifi cant (p=0.4526). However, the difference between the mean CI of males in both groups was not signifi cant (p=0.9535) likewise in females (p=0.3127). The mean head circumference in sickle cell disease children was 48.89±3.15 as against that of the normal growing non-sickle cell disease children 44.97±6.07 and this difference was also not statistically signifi cant (p=>0.05). Conclusion: The head shapes as per the present study could be classifi ed as mesocephalic in normal growing non-sickle cell disease children and brachycephalic in sickle cell disease children. Thus, it has been deduced that sickle cell disease could probably have an effect on head length, head width, cranial index and head circumference of affected children.  DOI: http://dx.doi.org/10.3126/ajms.v6i1.9160   Asian Journal of Medical Sciences Vol.6(1) 2015 98-102

scholarly journals Connecting the Neurobiology of Developmental Brain Injury: Neuronal Arborisation as a Regulator of Dysfunction and Potential Therapeutic Target

2021 ◽  
Vol 22 (15) ◽  
pp. 8220
Author(s):  
Ane Goikolea-Vives ◽  
Helen B. Stolp
Keyword(s):  
Neurodevelopmental Disorders ◽  
Synapse Formation ◽  
Neurodevelopmental Disorder ◽  
Therapeutic Benefit ◽  
Normal Brain ◽  
Environmental Pressures ◽  
Axon Extension ◽  
Neurodevelopmental Disease ◽  
Normal Brain Function ◽  
Pharmacological Modification

Neurodevelopmental disorders can derive from a complex combination of genetic variation and environmental pressures on key developmental processes. Despite this complex aetiology, and the equally complex array of syndromes and conditions diagnosed under the heading of neurodevelopmental disorder, there are parallels in the neuropathology of these conditions that suggest overlapping mechanisms of cellular injury and dysfunction. Neuronal arborisation is a process of dendrite and axon extension that is essential for the connectivity between neurons that underlies normal brain function. Disrupted arborisation and synapse formation are commonly reported in neurodevelopmental disorders. Here, we summarise the evidence for disrupted neuronal arborisation in these conditions, focusing primarily on the cortex and hippocampus. In addition, we explore the developmentally specific mechanisms by which neuronal arborisation is regulated. Finally, we discuss key regulators of neuronal arborisation that could link to neurodevelopmental disease and the potential for pharmacological modification of arborisation and the formation of synaptic connections that may provide therapeutic benefit in the future.

A Life Span Developmental Approach

2005 ◽  
Author(s):  
James C. Harris
Keyword(s):  
Intellectual Disability ◽  
Brain Development ◽  
Life Span ◽  
Cognitive Processing ◽  
Network Formation ◽  
Developmental Trajectories ◽  
Neurodevelopmental Disorder ◽  
Normal Brain ◽  
The Brain ◽  
Normal Brain Development

Intellectual disability is a neurodevelopmental disorder that continues throughout the life span of the affected person. It is essential to understand how persons with intellectual disability progress throughout their life span from infancy to old age. The maturation of the brain, their environmental experiences, and the mastery of developmental challenges and tasks must all be considered. A focus on brain development is in keeping with neuroscience research indicating that progressive brain maturation is accompanied by successive synaptic reorganization as one moves from one developmental stage to the next. Anatomical Magnetic Resonance Imaging Studies are playing a major role in understanding the developmental trajectories of normal brain development (Durston et al., 2001; Giedd et al., 1999). Understanding the developmental trajectories of normal brain development is crucial to the interpretation of brain development in neurodevelopmental disabilities. During normal development, white matter volume increases with age, and although gray matter volumes increase during childhood, they decrease before adulthood. These changes in the brain are accompanied by changes in cognitive processing; for example, executive functioning shows a progressive emergence from the preschool years (Espy et al., 1999) into the adolescent years. Working memory and inhibitory processes may be measured during the preschool years. By adolescence, abstract reasoning, anticipatory planning, and mental judgment have emerged and may be measured. Cognitive abilities in adolescence are qualitatively different from those of young children as a result of the reorganization of the prefrontal cortex during maturation. How genetic background and environment interact in producing these changes is the object of ongoing study, yet investigators are beginning to understand how physiological processes of synaptic development, circuits, and neuronal network formation relate to processes of cognitive development (Fossella et al., 2003). The development of persons with intellectual disability is now being evaluated systematically, and developmental trajectories are being established for known neurogenetic syndromes. These studies are making up for a surprising lack of application of a developmental perspective to persons with intellectual disability. Developmental theorists have, for the most part, monitored and measured development in normally intelligent persons in establishing developmental landmarks.

scholarly journals Regulation of Thyroid-disrupting Chemicals to Protect the Developing Brain

Endocrinology ◽  
2020 ◽  
Vol 161 (10) ◽  
Author(s):  
Mary E Gilbert ◽  
Katherine L O’Shaughnessy ◽  
Marta Axelstad
Keyword(s):  
Brain Development ◽  
Toxicity Testing ◽  
Children's Health ◽  
Children’S Health ◽  
Normal Brain ◽  
Synthetic Chemicals ◽  
Endocrine Disrupting ◽  
Brain Circuitry ◽  
Abnormal Brain

Abstract Synthetic chemicals with endocrine disrupting properties are pervasive in the environment and are present in the bodies of humans and wildlife. As thyroid hormones (THs) control normal brain development, and maternal hypothyroxinemia is associated with neurological impairments in children, chemicals that interfere with TH signaling are of considerable concern for children’s health. However, identifying thyroid-disrupting chemicals (TDCs) in vivo is largely based on measuring serum tetraiodothyronine in rats, which may be inadequate to assess TDCs with disparate mechanisms of action and insufficient to evaluate the potential neurotoxicity of TDCs. In this review 2 neurodevelopmental processes that are dependent on TH action are highlighted, neuronal migration and maturation of gamma amino butyric acid-ergic interneurons. We discuss how interruption of these processes by TDCs may contribute to abnormal brain circuitry following developmental TH insufficiency. Finally, we identify issues in evaluating the developmental neurotoxicity of TDCs and the strengths and limitations of current approaches designed to regulate them. It is clear that an enhanced understanding of how THs affect brain development will lead to refined toxicity testing, reducing uncertainty and improving our ability to protect children’s health.

scholarly journals Emerging Role of ODC1 in Neurodevelopmental Disorders and Brain Development

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 470
Author(s):  
Jeremy W. Prokop ◽  
Caleb P. Bupp ◽  
Austin Frisch ◽  
Stephanie M. Bilinovich ◽  
Daniel B. Campbell ◽  
...  
Keyword(s):  
Brain Development ◽  
Neural Progenitor Cells ◽  
Neurodevelopmental Disorder ◽  
Fetal Brain ◽  
Missense Variant ◽  
Neural Progenitor ◽  
Loss Of Function ◽  
Gain Of Function ◽  
Systematic Analysis ◽  
Function Expression

Ornithine decarboxylase 1 (ODC1 gene) has been linked through gain-of-function variants to a rare disease featuring developmental delay, alopecia, macrocephaly, and structural brain anomalies. ODC1 has been linked to additional diseases like cancer, with growing evidence for neurological contributions to schizophrenia, mood disorders, anxiety, epilepsy, learning, and suicidal behavior. The evidence of ODC1 connection to neural disorders highlights the need for a systematic analysis of ODC1 genotype-to-phenotype associations. An analysis of variants from ClinVar, Geno2MP, TOPMed, gnomAD, and COSMIC revealed an intellectual disability and seizure connected loss-of-function variant, ODC G84R (rs138359527, NC_000002.12:g.10444500C > T). The missense variant is found in ~1% of South Asian individuals and results in 2.5-fold decrease in enzyme function. Expression quantitative trait loci (eQTLs) reveal multiple functionally annotated, non-coding variants regulating ODC1 that associate with psychiatric/neurological phenotypes. Further dissection of RNA-Seq during fetal brain development and within cerebral organoids showed an association of ODC1 expression with cell proliferation of neural progenitor cells, suggesting gain-of-function variants with neural over-proliferation and loss-of-function variants with neural depletion. The linkage from the expression data of ODC1 in early neural progenitor proliferation to phenotypes of neurodevelopmental delay and to the connection of polyamine metabolites in brain function establish ODC1 as a bona fide neurodevelopmental disorder gene.

scholarly journals LSD1 enzyme inhibitor TAK-418 unlocks aberrant epigenetic machinery and improves autism symptoms in neurodevelopmental disorder models

2021 ◽  
Vol 7 (11) ◽  
pp. eaba1187
Author(s):  
Rina Baba ◽  
Satoru Matsuda ◽  
Yuuichi Arakawa ◽  
Ryuji Yamada ◽  
Noriko Suzuki ◽  
...  
Keyword(s):  
Gene Expression ◽  
Enzyme Activity ◽  
Neurodevelopmental Disorders ◽  
Neurodevelopmental Disorder ◽  
Specific Inhibitor ◽  
Autism Spectrum ◽  
Poly I:C ◽  
Control Of Gene Expression ◽  
Epigenetic Machinery ◽  
The Brain

Persistent epigenetic dysregulation may underlie the pathophysiology of neurodevelopmental disorders, such as autism spectrum disorder (ASD). Here, we show that the inhibition of lysine-specific demethylase 1 (LSD1) enzyme activity normalizes aberrant epigenetic control of gene expression in neurodevelopmental disorders. Maternal exposure to valproate or poly I:C caused sustained dysregulation of gene expression in the brain and ASD-like social and cognitive deficits after birth in rodents. Unexpectedly, a specific inhibitor of LSD1 enzyme activity, 5-((1R,2R)-2-((cyclopropylmethyl)amino)cyclopropyl)-N-(tetrahydro-2H-pyran-4-yl)thiophene-3-carboxamide hydrochloride (TAK-418), almost completely normalized the dysregulated gene expression in the brain and ameliorated some ASD-like behaviors in these models. The genes modulated by TAK-418 were almost completely different across the models and their ages. These results suggest that LSD1 enzyme activity may stabilize the aberrant epigenetic machinery in neurodevelopmental disorders, and the inhibition of LSD1 enzyme activity may be the master key to recover gene expression homeostasis. TAK-418 may benefit patients with neurodevelopmental disorders.

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