Neural tube defects, their implications and solutions in Muslim society

2020 ◽  
pp. 1-8
Author(s):  
Muhammad Fayyaz ◽  
Arshad Khushdil ◽  
Shehla Baqai
Keyword(s):  
Folic Acid ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Time Frame ◽  
Value Systems ◽  
Complex Issue ◽  
Empathic Understanding ◽  
The Given

Abstract Neural Tube Defects (NTDs) are serious congenital abnormalities and most of them are incompatible with life. The extremely debilitating quality of life, if one survives, calls for actions to prevent such sufferings.  Experts agree on the role of Folic Acid in primary prevention of NTDs, yet, despite best efforts, the use of Folic Acid has reduced NTDs by only 50%. These cases too can be prevented by employing secondary preventive measures. These involve timely interruption of pregnancy -- a decision which, in addition to a medical judgment, is based on ethics, social, cultural and Muslim religious value systems in Pakistan. Indeed, it is a complex issue but empathic understanding and strong co-ordination, once established between different disciplines, can help parents to decide and opt for necessary secondary prevention by interruption of malformed foetus within the given time frame mandated by medical and religious authorities. Continuous....

The Role of Folic Acid Fortification in Neural Tube Defects: A Review

2013 ◽  
Vol 53 (11) ◽  
pp. 1180-1190 ◽  
Author(s):  
Anja Osterhues ◽  
Nyima S. Ali ◽  
Karin B. Michels
Keyword(s):  
Folic Acid ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Folic Acid Fortification

scholarly journals METTL3-Mediated m6A Modification is Involved in Neural Tube Defects via Modulating Wnt/β-Catenin Signaling Pathway

2021 ◽  
Author(s):  
Li Zhang ◽  
Rui Cao ◽  
Dandan Li ◽  
Yuqing Sun ◽  
Juan Zhang ◽  
...  
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Theoretical Basis ◽  
Clinical Work ◽  
Folic Acid Deficiency ◽  
Acid Deficiency ◽  
Life Threatening ◽  
Neural Tube Development

Abstract Neural tube defects (NTDs) remain one of the most life-threatening birth defects affecting infants. Most patients with a NTDs eventually develop lifelong disability, which cause significant morbidity and mortality and seriously reduce the quality of life. Therefore, identifiable of novel pathogenic strategies for NTDs patients is urgently required. Increasing evidence indicates that METTL3-mediated m6A modification is present in many physiopathological processes of cell apoptosis and survival. Our results demonstrate that SAM play not only a compensatory role, SAM can also lead to m6A modification changes in neural tube development and regulation. This research provides a good theoretical basis for further research on folic acid deficiency leading to NTDs, reveals the important role of SAM in the development of NTDs, and provides new clue for clinical researchers and clinical work.

scholarly journals The role of folic acid in prevention of neural tube defects caused by high dose progesterone.

2011 ◽  
Author(s):  
Iram Iqbal ◽  
Khadija Qamar ◽  
Omar Hyder ◽  
Ifra Saeed ◽  
Umbreen Noor
Keyword(s):  
Folic Acid ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
High Dose

scholarly journals Reducing inequities in preventable neural tube defects: the critical and underutilized role of neurosurgical advocacy for folate fortification

2018 ◽  
Vol 45 (4) ◽  
pp. E20 ◽  
Author(s):  
Dagoberto Estevez-Ordonez ◽  
Matthew C. Davis ◽  
Betsy Hopson ◽  
Anastasia Arynchyna ◽  
Brandon G. Rocque ◽  
...  
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Implementation Strategies ◽  
Indirect Costs ◽  
Childhood Mortality ◽  
High Morbidity ◽  
Disability Adjusted Life ◽  
Life Years

Neural tube defects (NTDs) are one of the greatest causes of childhood mortality and disability-adjusted life years worldwide. Global prevalence at birth is approximately 18.6 per 10,000 live births, with more than 300,000 infants with NTDs born every year. Substantial strides have been made in understanding the genetics, pathophysiology, and surgical treatment of NTDs, yet the natural history remains one of high morbidity and profound impairment of quality of life. Direct and indirect costs of care are enormous, which ensures profound inequities and disparities in the burden of disease in countries of low and moderate resources. All indices of disease burden are higher for NTDs in developing countries. The great tragedy is that the majority of NTDs can be prevented with folate fortification of commercially produced food. Unequivocal evidence of the effectiveness of folate to reduce the incidence of NTDs has existed for more than 25 years. Yet, the most comprehensive surveys of effectiveness of implementation strategies show that more than 100 countries fail to fortify, and consequently only 13% of folate-preventable spina bifida is actually prevented. Neurosurgeons harbor a disproportionate, central, and fundamental role in the management of NTDs and enjoy high standing in society. No organized group in medicine can speak as authoritatively or convincingly. As a result, neurosurgeons and organized neurosurgery harbor disproportionate potential to advocate for more comprehensive folate fortification, and thereby prevent the most common and severe birth defect to impact the human nervous system. Assertive, proactive, informed advocacy for folate fortification should be a central and integral part of the neurosurgical approach to NTDs. Only by making the prevention of dysraphism a priority can we best address the inequities often observed worldwide.

scholarly journals Ethionine-mediated reduction of S-adenosylmethionine is responsible for the neural tube defects in the developing mouse embryo-mediated m6A modification and is involved in neural tube defects via modulating Wnt/β-catenin signaling pathway

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Li Zhang ◽  
Rui Cao ◽  
Dandan Li ◽  
Yuqing Sun ◽  
Juan Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Epigenetic Mechanism ◽  
Proliferation And Apoptosis ◽  
Life Threatening ◽  
Neural Tube Development

AbstractNeural tube defects (NTDs) remain one of the most life-threatening birth defects affecting infants. Most patients with NTDs eventually develop lifelong disability, which cause significant morbidity and mortality and seriously reduce the quality of life. Our previous study has found that ethionine inhibits cell viability by disrupting the balance between proliferation and apoptosis, and preventing neural stem cells from differentiating into neurons and astrocytes. However, how ethionine participates in the pathogenesis of neural tube development through N6-methyladenosine (m6A) modification remains unknown. This study aims to investigate METTL3- and ALKBH5-mediated m6A modification function and mechanism in NTDs. Herein, our results demonstrate that SAM play not only a compensatory role, it also leads to changes of m6A modification in neural tube development and regulation. Additionally, these data implicate that METTL3 is enriched in HT-22 cells, and METTL3 knockdown reduces cell proliferation and increases apoptosis through suppressing Wnt/β-catenin signaling pathway. Significantly, overexpression of ALKBH5 can only inhibit cell proliferation, but cannot promote cell apoptosis. This research reveals an important role of SAM in development of NTDs, providing a good theoretical basis for further research on NTDs. This finding represents a novel epigenetic mechanism underlying that the m6A modification has profound and lasting implications for neural tube development.

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