The main conclusions of this review are as follows: (i) the brain 5-HT deficiency contributes to the mechanism underlying SAD, (ii) TPH2 is involved in the regulation of some kinds of genetically defined affective disorders and (iii) the activation of 5-HT synthesis with exogenous l-tryptophan alone or in combination with light therapy could be effective in SAD treatment.
Genetic variation in human tryptophan hydroxylase 2 (TPH2) influences TPH enzymatic activity and is associated with emotion-related traits and mood disorders.
Genetic variation in human tryptophan hydroxylase 2 (TPH2) influences TPH enzymatic activity and is associated with emotion-related traits and mood disorders.
Findings from psychophysiological and functional imaging studies are indicative of various TPH2 polymorphisms directly influencing serotonergic function and thus impacting on mood disorders and on the response to antidepressant treatment.
Aberrant serotonergic functioning is strongly implicated in hyperphagia in PWS, and females with TPH2 T alleles may be at higher risk for affective or mood disorders.
Findings from psychophysiological and functional imaging studies are indicative of various TPH2 polymorphisms directly influencing serotonergic function and thus impacting on mood disorders and on the response to antidepressant treatment.
More comprehensive study of TPH2 genetics is needed to increase the clinical value of the enzyme as a predictor of affective disorder risk and efficacy of antidepressant drugs.
More comprehensive study of TPH2 genetics is needed to increase the clinical value of the enzyme as a predictor of affective disorder risk and efficacy of antidepressant drugs.
No association was detected between the rs4131347 (-C8347G) SNP in the promoter region of the TPH2 gene and mood disorders, suicidal behavior or monoamine function.
Haplotype-based analysis of TPH2 in patients with UP and BP disorder and controls from northern Swedish descent provides preliminary evidence for protective association in both disorders and thus supports a central role for TPH2 in the pathogenesis of affective disorders.
Haplotype-based analysis of TPH2 in patients with UP and BP disorder and controls from northern Swedish descent provides preliminary evidence for protective association in both disorders and thus supports a central role for TPH2 in the pathogenesis of affective disorders.