Association of C677T  polymorphism (rs1801133) in MTHFR gene with depression

Rai, Vandana

doi:10.14715/cmb/2017.63.6.13

Cited by 31 publications

(14 citation statements)

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“…Under pathological conditions, Hcy fails to be efficiently recycled and therefore accumulates in the blood, leading to hyperhomocystinemia. Hyperhomocystinemia may increase the risk of various diseases, such as cardiovascular disorders, pulmonary embolism, and depression [24-26]. In our study, the serum level of Hcy in CAD patients was significantly higher than non-CAD controls, which supports the notion that hyperhomocystinemia might be involved in the pathogenesis of CAD.…”

Section: Discussionsupporting

confidence: 85%

A Case-Control Study of the Association of the Polymorphisms of MTHFR and APOE with Risk Factors and the Severity of Coronary Artery Disease

et al. 2019

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Objectives: To explore the association between single-nucleotide polymorphisms (SNPs) in MTHFR and APOE and the risk of CAD and, more importantly, the severity of CAD and the profile of serum lipids, we performed a case-control study in a Chinese Han population. Methods: A total of 1,207 cases of consecutive CAD-suspected inpatients were recruited, and 406 CAD cases and 231 non-CAD controls were enrolled for the final analysis after screening for exclusion criteria. All subjects had undergone coronary angiography, and the severity of CAD was evaluated by 2 cardiologists according to the Gensini scores. The genotypes of MTHFR and APOEwere detected using real-time PCR, and then verified by Sanger sequencing. Environmental risk factors, such as age, sex, smoking, alcohol consumption, hypertension, diabetes, dyslipidemia, and BMI were collected. Statistical analyses (the χ² test, binary logistic regression analysis, and ordinal polytomous logistic regression analysis) were performed with SPSS v16.0. Results: The genotypes ofall the subjects included in the CAD and non-CAD groups in this study were successfully detected, with an agreement of 100% with Sanger sequencing. The distributions of genotypes CT and TT at MTHFR C667T were higher in CAD cases than in non-CAD controls (OR 1.99, 95% CI 1.34–2.95; OR 1.77, 95% CI 1.18–2.67; p < 0.05), whereas genotype AC at MTHFR A1298Cwas lower in CAD cases (OR 0.71, 95% CI 0.50–1.02; p < 0.05). A significant association was observed in genotypes CT and TT at MTHFR C667T and the risk of CAD (OR 1.44, 95% CI 1.27–3.67; OR 1.56, 95% CI 0.88–2.78; p < 0.05). Both genotypes and alleles of APOE were comparable in the CAD cases and non-CAD controls (p > 0.05). The genotype TT at MTHFR C667T and ε4+ at APOE were more likely to be found in the CAD subgroup with a Gensini score ≥72 (p = 0.040 and p = 0.028, respectively). Meanwhile, in the patients with genotype TT,a higher level of serum Hcy was detected, while genotype ε4+ patients possessed higher levels of serum apolipoprotein E (ApoE) and low-density lipoprotein cholesterol (LDL-C) than other genotypes. Conclusion: This study revealed that the SNP site of MTHFR C667Tis associatedwith the risk of CAD in this Chinese Han population. In addition, the genotypes of TT in MTHFR C667T and ε4+in APOE may increase the severity of CAD, and higher Hcy, LDL-C, and ApoE levels may be involved in this pathogenic process.

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Section: Discussionsupporting

confidence: 85%

A Case-Control Study of the Association of the Polymorphisms of MTHFR and APOE with Risk Factors and the Severity of Coronary Artery Disease

et al. 2019

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“…The presence of the homozygous polymorphism c.665C>T on the MTHFR gene has been associated with hyperhomocysteinemia and a risk of thrombosis, depression, and carotid atherosclerosis [ 24 , 25 , 26 ]. It is possible that elevated levels of C-reactive protein reflect a proinflammatory status.…”

Section: Discussionmentioning

confidence: 99%

Metabolic Serendipities of Expanded Newborn Screening

Yahyaoui

Blasco‐Alonso

Gonzalo-Marín

et al. 2020

Genes

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Incidental findings on newborn screening (NBS) are results that are not the target of screening within a given NBS program, but rather are found as a result of the screening and resulting diagnostic workup for that target. These findings may not have an immediate clinical impact on the newborn, but are sometimes an additional benefit of NBS programs and may be considered secondary targets of NBS programs. This work describes four case reports that had incidental findings on the NBS, which eventually led to the diagnosis of another metabolic disease instead of the one that was initially suspected. The first case was a new defect in the cationic amino acid transporter-2 (CAT-2), which was oriented as an arginase-1 deficiency in the newborn. The second case was a maternal glutaric aciduria type 1 (GA-1) that mimicked a carnitine transporter deficiency in the newborn. The third report was a case of lysinuric protein intolerance (LPI), which appeared as high levels of citrulline on the NBS. The fourth case was a mother with homocystinuria that was diagnosed during the biochemical study of vitamin B12 status. All cases provide new or interesting data that will help guide differential diagnosis in the future.

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“…Folate, otherwise known as vitamin B9, comes in 2 forms: as dihydrofolate (in foods) or in a synthetic form (supplements). The first step in this one-carbon metabolism is the conversion of synthetic or dietary folate to 5-methyltetrahydrofolate (L-methylfolate) via methylenetetrahydrofolate reductase (MTHFR) [ 100 , 101 , 102 , 103 , 104 , 105 , 106 ]. L-methylfolate (also known as levomefolic acid or 5-methyltetrahydrofolate) is the active form of folate or folic acid and plays a critical role in the synthesis of neurotransmitters.…”

Section: Folic Acidmentioning

confidence: 99%

“…Methionine then reacts with ATP to form SAMe. SAMe acts as a methyl donor, similarly to L-methylfolate, and plays a critical role in the methylation of monoamines and, therefore, the synthesis of neurotransmitters via the tetrahydrobiopterin (BH4) pathway and the hydroxylation of phenylalanine and tryptophan [ 100 , 101 , 102 , 103 , 104 , 105 , 106 , 107 ]. The folic acid pathway is illustrated in Figure 1 below.…”

Section: Folic Acidmentioning

confidence: 99%

Treatment-Resistant Depression Revisited: A Glimmer of Hope

Halaris

Sohl

Whitham

2021

JPM

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Major Depressive Disorder (MDD) is a highly prevalent psychiatric disorder worldwide. It causes individual suffering, loss of productivity, increased health care costs and high suicide risk. Current pharmacologic interventions fail to produce at least partial response to approximately one third of these patients, and remission is obtained in approximately 30% of patients. This is known as Treatment-Resistant Depression (TRD). The burden of TRD exponentially increases the longer it persists, with a higher risk of impaired functional and social functioning, vast losses in quality of life and significant risk of somatic morbidity and suicidality. Different approaches have been suggested and utilized, but the results have not been encouraging. In this review article, we present new approaches to identify and correct potential causes of TRD, thereby reducing its prevalence and with it the overall burden of this disease entity. We will address potential contributory factors to TRD, most of which can be investigated in many laboratories as routine tests. We discuss endocrinological aberrations, notably, hypothalamic-pituitary-adrenal (HPA) axis dysregulation and thyroid and gonadal dysfunction. We address the role of Vitamin D in contributing to depression. Pharmacogenomic testing is being increasingly used to determine Single Nucleotide Polymorphisms in Cytochrome P450, Serotonin Transporter, COMT, folic acid conversion (MTHFR). As the role of immune system dysregulation is being recognized as potentially a major contributory factor to TRD, the measurement of C-reactive protein (CRP) and select immune biomarkers, where testing is available, can guide combination treatments with anti-inflammatory agents (e.g., selective COX-2 inhibitors) reversing treatment resistance. We focus on established and emerging test procedures, potential biomarkers and non-biologic assessments and interventions to apply personalized medicine to effectively manage treatment resistance in general and TRD specifically.

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Association of C677T polymorphism (rs1801133) in MTHFR gene with depression

Cited by 31 publications

References 0 publications

A Case-Control Study of the Association of the Polymorphisms of <b><i>MTHFR</i></b> and <b><i>APOE</i></b> with Risk Factors and the Severity of Coronary Artery Disease

A Case-Control Study of the Association of the Polymorphisms of <b><i>MTHFR</i></b> and <b><i>APOE</i></b> with Risk Factors and the Severity of Coronary Artery Disease

Metabolic Serendipities of Expanded Newborn Screening

Treatment-Resistant Depression Revisited: A Glimmer of Hope

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