Open AccessThe impact of dystrobrevin‐binding protein 1 ( DTNBP1 ) on neural correlates of episodic memory encoding and retrieval
Author(s) -
Thimm Markus,
Krug Axel,
Markov Valentin,
Krach Sören,
Jansen Andreas,
Zerres Klaus,
Eggermann Thomas,
Stöcker Tony,
Shah Nadim Jon,
Nöthen Markus M.,
Rietschel Marcella,
Kircher Tilo
Publication year - 2010
Publication title -
human brain mapping
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.005
H-Index - 191
eISSN - 1097-0193
pISSN - 1065-9471
DOI - 10.1002/hbm.20857
Subject(s) - cuneus , episodic memory , inferior parietal lobule , psychology , neuroscience , inferior frontal gyrus , prefrontal cortex , superior frontal gyrus , medial frontal gyrus , functional magnetic resonance imaging , brain activity and meditation , hippocampus , cognition , precuneus , electroencephalography
Episodic memory impairment is a frequently reported symptom in schizophrenia. It has been shown to be associated with reduced neural activity of the hippocampus and prefrontal cortex. Given the high heritability of schizophrenia the question arises if alterations in brain activity are modulated by susceptibility genes and might be detectable in healthy risk allele carriers. The present study investigated the effect of the single nucleotide polymorphism (SNP) rs1018381 (P1578) of the dystrobrevin‐binding protein 1 ( DTNBP1 ) on brain activity in 84 healthy subjects assessed by functional magnetic resonance imaging (fMRI) while they performed an episodic memory task comprising encoding and retrieval of faces. During encoding, the group of risk allele carriers ( n = 29) showed enhanced neural activity in the left middle frontal gyrus (BA 11) and bilaterally in the cuneus (BA 17, 7) when compared with the nonrisk carrier group ( n = 55). During retrieval, the risk group (compared to the non risk group) showed increased right hemispheric neural activity comprising the medial frontal gyrus (BA 9), inferior frontal gyrus (BA 9), and inferior parietal lobule (BA 40). Since there were no behavioral performance differences, increased neural activity of the risk group might be interpreted as a correlate of higher effort or differing cognitive strategies in order to compensate for a genetically determined slight cognitive deficit. Interestingly, the laterality of increased prefrontal activity is in accordance with the well known hemispheric encoding/retrieval asymmetry (HERA) model of episodic memory. Hum Brain Mapp, 2010. © 2009 Wiley‐Liss, Inc.