@article{3157210,
    title = "COMT and MTHFR polymorphisms interaction on cognition in schizophrenia:
An exploratory study",
    author = "Kontis, Dimitrios and Theochari, Eirini and Fryssira, Helen and Kleisas, and Spyridon and Sofocleous, Christalena and Andreopoulou, Angeliki and and Kalogerakou, Stamatina and Gazi, Anthia and Boniatsi, Lucia and and Chaidemenos, Alexandros and Tsaltas, Eleftheria",
    journal = "Neuroscience Letters",
    year = "2013",
    volume = "537",
    pages = "17-22",
    publisher = "Elsevier Ireland Ltd",
    issn = "0304-3940",
    doi = "10.1016/j.neulet.2013.01.012",
    keywords = "COMT; MTHFR; Schizophrenia; Cognition; CANTAB; Interaction",
    abstract = "The investigation of the catechol-O-methyltransferase (COMT-[rs4680])
and methylenetetrahydrofolate reductase (MTHFR-[rs1801133])
polymorphisms’ interaction might shed light into the pathogenetic
mechanisms of the cognitive dysfunction in schizophrenia. In an
exploratory study, we hypothesized that the MTHFR 677T allele which has
been related to a hypoactive MTHFR enzyme would augment the unfavorable
effects of COMT Val158 homozygosity which has been associated with COMT
enzyme hyperfunction. 90 schizophrenia patients and 55 healthy
volunteers were assessed on psychomotor speed, pattern and spatial
recognition memory (SRM), spatial working memory (SWM), attentional
flexibility and planning (Stockings of Cambridge-SOC). IQ scores in a
random subgroup of patients were also measured. A significant COMT x
MTHFR interaction on SWM (p = 0.048) and planning (p = 0.026) was
revealed in both groups. Among COMT-Val/Val participants, MTHFR-C/C made
more SWM errors (p = 0.033) and solved fewer SOC problems (p = 0.025)
than MTHFR-T carriers. In patients, there was a significant COMT x MTHFR
interaction on full scale IQ (p = 0.035): among COMT-Met carriers,
MTHFR-T carriers performed significantly worse than MTHFR-C/C (p =
0.021), which was driven by a COMT x MTHFR interaction involving
performance IQ(p = 0.047). In conclusion, COMT and MTHFR polymorphisms
interacted on cognition, suggesting that the MTHFR enzyme activity might
moderate the effects of the COMT enzyme. In contrast to our initial
hypothesis, the MTHFRT-allele attenuated the cognitive effects of COMT
Val homozygosity. In this preliminary study, we propose that
dopaminergic and intracellular methylation mechanisms could interact on
cognitive deficits in schizophrenia. (c) 2013 Elsevier Ireland Ltd. All
rights reserved."
}