2013
Interactive effect of MTHFR and ADRA2A gene polymorphisms on pathogenesis of schizophrenia
LOCHMAN, Jan; Jiří PLESNÍK; Vladimír JANOUT; Jana POVOVÁ; Ivan MÍŠEK et al.Základní údaje
Originální název
Interactive effect of MTHFR and ADRA2A gene polymorphisms on pathogenesis of schizophrenia
Autoři
Vydání
Neuroendocrinology Letters, Edition Medizin, 2013, 0172-780X
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30105 Physiology
Stát vydavatele
Lucembursko
Utajení
není předmětem státního či obchodního tajemství
Impakt faktor
Impact factor: 0.935
Označené pro přenos do RIV
Ano
Kód RIV
RIV/00216224:14310/13:00071796
Organizační jednotka
Přírodovědecká fakulta
UT WoS
Klíčová slova anglicky
MTHFR; COMT; ADRA2A; schizophrenia; association; polymorphism
Změněno: 28. 4. 2014 15:35, Ing. Andrea Mikešková
Anotace
V originále
Increasing evidences support the importance of epigenetic control in schizophrenia pathogenesis. One of the enzymes involved in DNA methylation process through homocysteine metabolism is methylenetetrahydrofolate reductase (MTHFR). The most extensively studied variant in the MTHFR gene is the C677T polymorphism, resulting in reduced enzyme activity and elevated homocysteine level. Methods: In sample of 192 schizophrenics and 213 healthy controls an increasing risk of schizophrenia associated with MTHFR 677 CT + TT genotype was found (OR=1.6, P=0.021). Association was also evaluated by considering the C677T polymorphism as an interaction with COMT Val158Met and ADRA2A C-1291G polymorphisms previously associated with schizophrenia risk using a logistic regression analysis. Results: Previous studies of MTHFR*COMT (C677T*Val158Met) interaction in relation to schizophrenia resulted in inconsistent results. In our sample this interaction did not significantly differ between schizophrenics and control subjects. On the other hand analysis of MTHFR*ADRA2A (C677T*C-1291G) interaction revealed significant association between ADRA2A CC+CG genotype in the MTHFR TC+TT carriers (P=0.008). Conclusions: Our results support role of noradrenergic functions as well as previously proposed role of epigenetic control in the pathogenesis of schizophrenia. Further relevant studies including larger sample size and more markers are needed to prove our results.