The Relationship between Dopamine Beta Hydroxylase Polymorphisms and Attenuated Psychotic Symptoms in Putatively Prodromal Adolescents Public
Ko, Chanyoung (2011)
Abstract
Abstract
Elevated dopamine in the subcortical regions of the brain such
as the striatum is strongly
associated with vulnerability to psychotic symptoms. The neural
mechanisms of elevated
subcortical dopamine remain ambiguous. Dysregulation of dopamine
beta hydroxylase (DBH) is
one possible contributor to abnormal dopamine levels. One
functional single nucleotide
polymorphism (SNP) at the DBH gene, -1021C->T, has shown to
affect DBH enzyme activity in
plasma and cerebrospinal fluid (CSF). The TT genotype of
-1021C->T, in particular, has been
associated with low DBH enzyme activity. Previous studies suggest
that lower DBH activity
may contribute to elevated DA levels, which in turn may increase
the vulnerability for
developing psychotic symptoms. Participants were administered the
Scale for Prodromal
Symptoms (SOPS) as a measure of prodromal symptom severity. Each
participant also provided
a saliva sample for DNA extraction. On all four SOPS prodromal
symptom scores, there was no
significant difference between individuals who are homozygous C and
T allele carriers at -
1021C->T. Furthermore, there were no significant differences
among the three genotypes (CC,
CT, and TT) in severity of prodromal symptoms. Though not reaching
statistical significance,
"T carriers" and TT genotype prodromal individuals showed a trend
toward greater positive
symptom severity compared to the CC genotype adolescents. Such
findings that individuals with
the DBH SNP associated with low DBH levels have greater
vulnerability for developing
psychotic symptoms are consistent with previous literature. Current
findings did not reach
statistical significance, suggesting that the present sample size
was not sufficient to detect effects
of the DBH SNP -1021C->T alone on prodromal symptoms in
adolescents at high-risk for
developing psychosis. It is likely that the young age of the sample
at follow-up contributed to
the lower conversion rate.
Table of Contents
TABLE OF CONTENTS
INTRODUCTION (1)
Schizophrenia: Phenomenology and Hypothesized Etiology (2)
The Psychosis Prodrome (7)
Dopamine Beta Hydroxylase (8)
CURRENT STUDY (14)
METHOD (15)
Participants (15)
Procedures (17)
Clinical Measures (17)
DNA Collection and Extraction (19)
RESULTS (20)
Symptom Severity by Diagnostic Groups (23)
Symptom Severity by Genotype (T carrier vs. homozygous C)
(24)
Conversion Status by Genotype (T carrier vs. homozygous C)
(25)
DISCUSSION (26)
REFERENCES (32)
TABLES (39)
FIGURES (48)
LIST OF TABLES
1 Clinical and Demographic Characteristics (39)
2 Clinical and Demographic Characteristics (1021C/T Genotypes)
(40)
3 Clinical and Demographic Characteristics (Homozygous C and T
carriers) (41)
4 Genotype Frequencies (1021C/T) in the Sample (42)
5 Genotype Frequencies by Diagnostic Groups (43)
6 Conversion Diagnoses by Diagnostic Groups (44)
7 Conversion Diagnoses by Genotype (Collapsed) (45)
8 Conversion Diagnoses by Genotype (Not collapsed) (46)
LIST OF FIGURES
1 Mean positive symptoms by DBH SNP groups (CC vs. T Carrier)
(48)
2 Mean negative symptoms by DBH SNP groups (CC vs. T Carrier)
(49)
3 Mean disorganized symptoms by DBH SNP groups (CC vs. T
Carrier)(50)
4 Mean general symptoms by DBH SNP groups (CC vs. T Carrier)
(51)
5 Conversion diagnoses by DBH SNP groups (CC vs. T Carrier)
(52)
6 Conversion diagnoses by DBH SNP genotypes (CC vs. CT vs. TT)
(53)
7 Mean positive symptoms by DBH SNP genotypes (54)
8 Mean negative symptoms by DBH SNP genotypes (55)
9 Mean disorganized symptoms by DBH SNP genotypes (56)
10 Mean general symptoms by DBH SNP genotypes (57)
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