TY - JOUR
TI - COMT and MTHFR polymorphisms interaction on cognition in schizophrenia:
An exploratory study
AU - Kontis, Dimitrios
AU - Theochari, Eirini
AU - Fryssira, Helen
AU - Kleisas,
AU - Spyridon
AU - Sofocleous, Christalena
AU - Andreopoulou, Angeliki and
AU - Kalogerakou, Stamatina
AU - Gazi, Anthia
AU - Boniatsi, Lucia and
AU - Chaidemenos, Alexandros
AU - Tsaltas, Eleftheria
JO - Neuroscience Letters
PY - 2013
VL - 537
TODO - null
SP - 17-22
PB - Elsevier Ireland Ltd
SN - 0304-3940
TODO - 10.1016/j.neulet.2013.01.012
TODO - COMT; MTHFR; Schizophrenia; Cognition; CANTAB; Interaction
TODO - 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.
ER -