Catechol-o-methyl transferase (COMT) val158met polymorphism and adolescent cortical development in patients with childhood-onset schizophrenia, their non-psychotic siblings, and healthy controls.

paper Cited Public

Authors: Raznahan, Armin; Greenstein, Deanna; Lee, Yohan; Long, Robert; Clasen, Liv; Gochman, Pete; Addington, Anjene; Giedd, Jay N; Rapoport, Judith L; Gogtay, Nitin
Year: 2011
Journal: NeuroImage
PMID: 21620981
DOI: 10.1016/j.neuroimage.2011.05.032
PMCID: PMC3285479

Fig. 1

Lateral and medial views of the cortical surface summarizing regions where Val158Met genotype was associated with significant (FDR corrected q < 0.05) difference in the rate of CT loss in Healthy Controls (HCs). Colored regions indicate where HCs show a step-wise reduction in the rate of CT loss for each extra Val allele. The inset plot illustrates this for the left dorsolateral prefrontal cortex.

Fig. 2

Regions where the relationship between COMT Val158Met Val allele dose and cortical thickness change is significantly different in healthy controls (HCs) as compared to probands with Childhood Onset Schizophrenia (COS). The inset plot illustrates this interaction for the left dorsolateral prefrontal region, where increased Val dose attenuates cortical thinning on HCs, but accelerates it in probands with COS. Note that by adulthood, COS Val homozygotes have persistent cortical thickness deficits compared to HCs, whereas Met homozygotes do not. All colored regions shown survive False Discovery Rate correction for multiple comparisons at q < 0.05.

Fig. 3

Regions where the relationship between COMT Val158Met Val allele dose and cortical thickness change is significantly different in healthy controls (HCs) as compared to the unaffected siblings (SIBs) of probands with schizophrenia. The inset plot illustrates this interaction for the left inferior temporal region, where increased Val dose attenuates cortical thinning on HCs, but accelerates it in SIBs. Note that by adulthood, cortical thickness trajectories have converged between HC and SIB groups—regardless of Val dose. All colored regions shown survive False Discovery Rate correction for multiple comparisons at q < 0.05.

#	Section	Preview
0	Introduction	Schizophrenia is a highly heritable (Cardno et al., 1999) neurodevelopmental disorder that is…
1	Introduction	Since DA is known to influence cellular processes fundamental to structural development of the…
2	Introduction	that these normative gene–brain relationships would be disrupted in patients with COS. We also…
3	Introduction	Catechol-o-methyltransferase has been intensely investigated in schizophrenia genetics as a…
4	Introduction	tissue (Chen et al., 2004). Increased DA catabolism imparted by the Val allele is thought to result…
5	Introduction	Cortical thickness (CT) was studied as a developmentally sensitive (Raznahan et al., 2010) sMRI…
6	Materials and methods — Subjects	Subject characteristics are summarized in Table 1, and detailed in supplementary on-line material…
7	Materials and methods — Controls	We included 208 healthy controls (HCs), with a total of 475 structural magnetic resonance imaging…
8	Materials and methods — COS subjects and their non-psychotic siblings	Patients with COS were recruited through nationwide referral and extensive prescreening. Diagnoses…
9	Materials and methods — Genotyping	DNA was extracted from previously prepared lymphoblastoid cell lines using standard methods (Qiagen,…
10	Materials and methods — Neuroimaging	Of all 353 participants, 67% had 2 or more scans and 42% had 3 or more brain MRI scans acquired at…
11	Materials and methods — Neuroimaging	for non-uniformity artifacts (Sled et al., 1998); and image classification into white matter, grey…
12	Materials and methods — Neuroimaging	surface. In the absence of prior evidence regarding the spatial extent of genotype effects on…
13	Materials and methods — Statistical analysis	In line with molecular data (Chen et al., 2004), and previous imaging-genetic studies (Egan et al.,…
14	Materials and methods — Statistical analysis	In all analyses, mixed models were run separately at each vertex. We first established the…
15	Materials and methods — Statistical analysis	Regions where the t-statistic associated with the β4 coefficient (differences in the rate of CT…
16	Materials and methods — Statistical analysis	Then, to contrast the relationship between Val158Met genotype and cortical development between…
17	Materials and methods — Statistical analysis	This model was run once for each possible contrast between the three clinical groups: HC, COS…
18	Results	Sample demographics are summarized in Table 1 (and detailed in Supplementary Table 1). There were…
19	Results	Subsidiary analyses were conducted to investigate the possibility of confounds arising from HCs…

Name	Type
abnormal brain anatomical change local	phenotype
activational efficiency local	phenotype
adolescent cortical thickness loss local	phenotype
anterior cingulate cortex	anatomy
bilateral cingulate local	anatomy
bilateral inferior frontal gyrus local	anatomy
brain	anatomy
brain development	phenotype
cerebral hemispheres	anatomy
cerebrospinal fluid	drug
childhood-onset schizophrenia local	cohort
childhood-onset schizophrenia local	phenotype
Childhood-onset schizophrenia local	cohort
Childhood-onset schizophrenia local	phenotype
children with schizophrenia local	cohort
cingulate cortex	anatomy
Clinical Group local	cohort
COMT	gene
COMT Val158	gene
COMT Val158Met	gene
cortex	anatomy
cortical D1 density local	phenotype
cortical DA signaling local	phenotype
cortical dysmaturation local	phenotype
cortical folding patterns local	phenotype
cortical function	phenotype
cortical hypodopaminergia local	phenotype
cortical maturation local	phenotype
Cortical maturation local	phenotype
Cortical structure local	phenotype
cortical surface	anatomy
cortical thickness	phenotype
cortical thickness change local	anatomy
Cortical thickness change local	phenotype
cortical thickness deficits local	phenotype
Cortical thickness maturation local	phenotype
COS local	cohort
COS local	phenotype
COS probands local	cohort
CSF local	anatomy
CT	phenotype
CT deficits local	phenotype
dlPFC	anatomy
dlPFC cortical thickness deficit local	phenotype
dopamine	drug
dopamine dysregulation local	phenotype
dopamine-modifying drugs local	drug
Dopaminergic dysregulation local	phenotype
Dopamine signaling genetic variants local	variant
dorsolateral prefrontal cortex	anatomy
DRD2	gene
executive function	phenotype
exploitative behavior local	phenotype
exploratory behavior	phenotype
families	cohort
Family history cohort local	cohort
Fronto-temporal cortex local	anatomy
fronto-temporal gray matter deficit local	phenotype
Fronto-temporal sub-regions local	anatomy
full-scale IQ	phenotype
functional abnormalities	phenotype
functional interconnectivity local	phenotype
Genetic liability for schizophrenia local	phenotype
genetic risk	cohort
genetic variant impacting dopamine signaling local	variant
gray matter	anatomy
gray/pial surface local	anatomy
gray/white boundary	anatomy
gyrification local	phenotype
HC	cohort
hCS	cohort
healthy brain development local	phenotype
healthy controls	cohort
higher associative cortices local	anatomy
high-risk offspring	cohort
inferior temporal cortex local	anatomy
intellectual ability local	phenotype
inter-neuron differentiation local	phenotype
language	phenotype
lateral prefrontal cortex	anatomy
Lateral temporal region local	anatomy
lateral temporal regions local	anatomy
left dlPFC	anatomy
left intraparietal sulcus local	anatomy
lymphoblastoid cell lines	cohort
mean age	phenotype
medPFC local	anatomy
meso-cortical circuit local	anatomy
meso-limbic circuit local	anatomy
meso-striatal circuit local	anatomy
Met allele local	variant
MetMet genotype local	variant
Middle cingulate cortex local	anatomy
MNI-ICBM152 Stereotaxic Space local	anatomy
neurogenesis	phenotype
neuronal differentiation	phenotype
non-psychotic siblings local	cohort
Non-psychotic siblings local	cohort
non-white groups local	phenotype
oscillatory activity	phenotype
Parietal associative cortices local	anatomy
parietal cortex	anatomy
Performance IQ	phenotype
persistent cortical thickness deficits local	phenotype
persistent fronto-temporal gray matter deficit local	phenotype
PFC	anatomy
PFC hypodopaminergia local	phenotype
prefrontal cortex	anatomy
probands	cohort
prodromal symptoms	phenotype
psychosis	phenotype
Race distribution local	phenotype
race/ethnicity	phenotype
reduced PFC functioning local	phenotype
rs4680	variant
schizophrenia	phenotype
sex	phenotype
SIB local	cohort
siblings	cohort
signal-to-noise ratio	phenotype
structural cortical deficits local	phenotype
Structural maturation abnormalities local	phenotype
structural MRI	drug
STS local	anatomy
study cohort	cohort
subjects	cohort
superior parietal cortex	anatomy
superior temporal cortex local	anatomy
surface area	phenotype
temporal cortex	anatomy
Twin cohort	cohort
typical development	phenotype
unaffected SIBs local	cohort
Val158 allele	gene
Val158Met	gene
Val158Met genotype local	variant
Val allele	gene
Val allele dosage local	variant
ValMet genotype local	variant
Valproic acid	drug
ValVal genotype local	variant
Velocardiofacial syndrome	phenotype
Verbal IQ local	phenotype
vocabulary	phenotype
white matter	anatomy
working memory	phenotype
β4 coefficient local	variant

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