Alleviating Oxidative Damage–Induced Telomere Attrition: a Potential Mechanism for Inhibition by Folic Acid of Apoptosis in Neural Stem Cells

Li, Zhenshu; Li, Wen; Zhou, Dezheng; Zhao, Jing; Ma, Yue; Huang, Ling; Dong, Cuixia; Wilson, John X.; Huang, Guowei

doi:10.1007/s12035-021-02623-3

Cited by 10 publications

(7 citation statements)

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“…Folic acid inhibits apoptosis of motoneuronal stem cells, alleviating telomere wear induced by oxidative damage. This effect and other protective effects indicate that supplementation of folic acid may be useful in patients with ALS [122].…”

Section: Thiamine or Vitamin B1mentioning

confidence: 83%

P53 Protein Modulates Muscle Metabolism and Generates a Non-Genetic Risk Environment that Contributes to Triggering Amyotrophic Lateral Sclerosis

Espina-Zambrano¹

2022

Preprint

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Amyotrophic lateral sclerosis (ALS) is also called "motor neuron disease”. In this review, we propose that ALS is not just a neuromotor disorder, but begins as a disorder of P53-modulated skeletal muscle metabolism, leading to failures at the energy state of the cells, incorrect redox states, motor denervation, and a loss of muscle fibers. Motoneurons die as a consequence of the lack of muscular feedback, and the oligomeric TDP43 aggregates progressively and relentlessly lead to mistakes in peripheral immune self-tolerance sustained over time. An effective treatment has not been found for this devastating pathology, as for 152 years the target has not been accurately defined. Scientists and doctors should consider new knowledge regarding ALS and consider immunomodulatory therapies that, based on genetic analysis and symptoms, can be combined with compounds that regulate metabolism and promote the elimination of useless organelles and cells. What if ALS could be cured as a result of seeing motor neuron disease differently? This review aims to develop that goal and change the paradigm of our understanding of ALS.

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Section: Thiamine or Vitamin B1mentioning

confidence: 83%

P53 Protein Modulates Muscle Metabolism and Generates a Non-Genetic Risk Environment that Contributes to Triggering Amyotrophic Lateral Sclerosis

Espina-Zambrano¹

2022

Preprint

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“…SparkJade) for 1 h. Images of cells were captured by an Olympus IX81 microscope. C-rich telomere probe-FITC (TelC-FITC) and DNA damage response protein γ-H2AX were considered telomere dysfunction-induced foci (TIF)-positive cells if there were more than two IF foci [ 26 ]. Telomere length and oxidative telomeric DNA damage were also analyzed using the Image J plugin Telometer as well.…”

Section: Methodsmentioning

confidence: 99%

Parental Folate Deficiency Inhibits Proliferation and Increases Apoptosis of Neural Stem Cells in Rat Offspring: Aggravating Telomere Attrition as a Potential Mechanism

et al. 2023

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The effect of maternal folate status on the fetal central nervous system (CNS) is well recognized, while evidence is emerging that such an association also exists between fathers and offspring. The biological functions of telomeres and telomerase are also related to neural cell proliferation and apoptosis. The study aimed to investigate the effect of parental folate deficiency on the proliferation and apoptosis of neural stem cells (NSCs) in neonatal offspring and the role of telomeres in this effect. In this study, rats were divided into four groups: maternal folate-deficient and paternal folate-deficient diet (D-D) group; maternal folate-deficient and paternal folate-normal diet (D-N) group; maternal folate-normal and paternal folate-deficient diet (N-D) group; and the maternal folate-normal and paternal folate-normal diet (N-N) group. The offspring were sacrificed at postnatal day 0 (PND0), and NSCs were cultured from the hippocampus and striatum tissues of offspring for future assay. The results revealed that parental folate deficiency decreased folate levels, increased homocysteine (Hcy) levels of the offspring’s brain tissue, inhibited proliferation, increased apoptosis, shortened telomere length, and aggravated telomere attrition of offspring NSCs in vivo and in vitro. In vitro experiments further showed that offspring NSCs telomerase activity was inhibited due to parental folate deficiency. In conclusion, parental folate deficiency inhibited the proliferation and increased apoptosis of offspring NSCs, maternal folate deficiency had more adverse effects than paternal, and the mechanisms may involve the telomere attrition of NSCs.

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“…Some studies have found that obesity has a stronger effect on TL in women than in men [69,70], while other studies have reported no effect on sex differences [65,71]. Several studies have examined the impact of stress, exercise, and food on TL [72][73][74]. Additionally, TL has been investigated in relation to psychological and behavioral elements.…”

Section: Telomere Lengthmentioning

confidence: 99%

Involvement of Inheritance in Determining Telomere Length beyond Environmental and Lifestyle Factors

Gold,

Okeke,

2023

Aging and disease

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All linear chromosomal ends have specific DNA-protein complexes called telomeres. Telomeres serve as a "molecular clock" to estimate the potential length of cell replication. Shortening of telomere length (TL) is associated with cellular senescence, aging, and various age-related diseases in humans. Here we reviewed the structure, function, and regulation of telomeres and the age-related diseases associated with telomere attrition. Among the various determinants of TL, we highlight the connection between TL and heredity to provide a new overview of genetic determinants for TL. Studies across multiple species have shown that maternal and paternal TL influence the TL of their offspring, and this may affect life span and their susceptibility to age-related diseases. Hence, we reviewed the linkage between TL and parental influences and the proposed mechanisms involved. More in-depth studies on the genetic mechanism for TL attrition are needed due to the potential application of this knowledge in human medicine to prevent premature frailty at its earliest stage, as well as promote health and longevity.

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Alleviating Oxidative Damage–Induced Telomere Attrition: a Potential Mechanism for Inhibition by Folic Acid of Apoptosis in Neural Stem Cells

Cited by 10 publications

References 50 publications

P53 Protein Modulates Muscle Metabolism and Generates a Non-Genetic Risk Environment that Contributes to Triggering Amyotrophic Lateral Sclerosis

P53 Protein Modulates Muscle Metabolism and Generates a Non-Genetic Risk Environment that Contributes to Triggering Amyotrophic Lateral Sclerosis

Parental Folate Deficiency Inhibits Proliferation and Increases Apoptosis of Neural Stem Cells in Rat Offspring: Aggravating Telomere Attrition as a Potential Mechanism

Involvement of Inheritance in Determining Telomere Length beyond Environmental and Lifestyle Factors

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