Methylenetetrahydrofo late reductase C677T polymorphism and schizophrenia: Effect of molecular change
Sora Yasri1, Viroj Wiwanitkit2
1 KMT Primary Care Center, Bangkok, Thailand
2 Tropical Medicine, Hainan Medical University, Haikou, China
|Date of Web Publication||27-Mar-2018|
Dr. Sora Yasri
KMT Primary Care Center, Bangkok
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Yasri S, Wiwanitkit V. Methylenetetrahydrofo late reductase C677T polymorphism and schizophrenia: Effect of molecular change. J Res Med Sci 2018;23:20
|How to cite this URL:|
Yasri S, Wiwanitkit V. Methylenetetrahydrofo late reductase C677T polymorphism and schizophrenia: Effect of molecular change. J Res Med Sci [serial online] 2018 [cited 2020 Feb 26];23:20. Available from: http://www.jmsjournal.net/text.asp?2018/23/1/20/228592
Schizophrenia is an important psychological disorder. There are many reports on the underlying medical and genetic underlying factors of schizophrenia. Malhotra et al. recently noted that“there is some evidence to suggest an association of MetS with adiponectin levels, hematological indices, methylenetetrahydrofolate reductase (MTHFR), and Alpha-1A adrenergic receptor gene.” Focusing on MTHFR, Yadav et al. performed meta-analysis study and suggested that “the MTHFR C677T polymorphism is a risk factor for schizophrenia.” Here, the authors would like to discuss on the effect of MTHFR C677T polymorphism based on basic consideration on nanomolecular weight change. Theoretically, the molecule with polymorphism will have altered molecular weight that might affect the biological process. Using the quantum calculation technique as previously reported in the previous publications,,, it can be seen that the C677T polymorphism has a lower molecular weight than wild-type (decreased mass = 2). Per one molecule, the decreased molecular weight in the mutated polymorphism will result in a less mass of final biochemical product comparing to naïve type. Indeed, this finding is concordant with a previous observation that MTHFR deficit could induce schizophrenia. The important key message is the decreased molecular mass in C677T polymorphism can imply reduced MTHFR activity that can be an explanation for the observed relationship to schizophrenia.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Malhotra N, Grover S, Chakrabarti S, Kulhara P. Metabolic syndrome in schizophrenia. Indian J Psychol Med 2013;35:227-40.
] [Full text]
Yadav U, Kumar P, Gupta S, Rai V. Role of MTHFR C677T gene polymorphism in the susceptibility of schizophrenia: An updated meta-analysis. Asian J Psychiatr 2016;20:41-51.
Joob B, Wiwanitkit V. HSD11B1 rs846908 polymorphisms and tacrolimus concentrations: Quantum chemical analysis and implication in patients with renal transplantation. J Nephropharmacol 2017;6:19-20.
Joob B, Wiwanitkit V. ATP-binding cassette, sub-family B (MDR/TAP), member 1 (ABCB1) polymorphism and clopidogrel concentration in acute coronary syndrome: Molecular change can explain the observed therapeutic concentration. Anatol J Cardiol 2016;16:303-4.
Wiwanitkit S, Wiwanitkit V. Change in molecular weight due to important pfatp6 and pfmdr1 polymorphisms and susceptibility to antimalarial drug: Possible role of epigenetic phenomenon. Asian Pac J Trop Biomed 2017;7:181-2.
Wang Q, Liu J, Liu YP, Li XY, Ma YY, Wu TF, et al.
Methylenetetrahydrofolate reductase deficiency-induced schizophrenia in a school-age boy. Zhongguo Dang Dai Er Ke Za Zhi 2014;16:62-6.