Compound S6, characterized by partial D<sub>2</sub> R agonism, 5-HT<sub>1A</sub> R agonism, 5-HT<sub>2A</sub> R antagonism, and blockade of SERT activities, was found to decrease psychosis- and depressive-like symptoms in rodents.
The polypharmacology profile of 62, characterized by partial 5-HT<sub>1A</sub>R agonism, 5-HT<sub>2A</sub>/5-HT<sub>7</sub>/D<sub>2</sub>/D<sub>3</sub>R antagonism, and blockade of SERT, reduced the "positive"-like, and "negative"-like symptoms of psychoses.
Therefore, anxiety and depressive disorders are treated by SSRIs which inhibit serotonin transporter (5-HTT) while psychotic disorders are controlled by drugs that block serotonin and/or dopamine receptors.
To examine the role of 5-HTTLPR, rs25531 and 5-HTT VNTR Intron 2 variants in subjects with psychotic disorders manifesting suicide ideation and behaviour.
We hypothesize that 5-HTTLPR variations and long-term effects of childhood trauma interact and contribute to some of the variation in cognitive dysfunction seen in patients with psychotic disorders.
However, significant associations were observed between 5-HTT-LPR variants and early negative symptom response among first-episode patients with psychosis.
The serotonin transporter gene and disease modification in psychosis: evidence for systematic differences in allelic directionality at the 5-HTTLPR locus.
We observed significant genotypic association of the 5-HTTLPR polymorphism with MAP psychosis (P= 0.022), particularly in patients who show prolonged psychosis.
In the present study, we investigated the effects of the 44 bp insertion/deletion polymorphism in the promoter region of 5-HTT gene (5-HTTLPR) on symptomatology of psychosis and clinical response to antipsychotic drugs.
No significant differences in the distribution of allele and genotype frequencies of the 5-HTTLPR (p>0.01) and 5-HT2A T102C (p>0.05) were found between patients and controls as well as between the patients' subgroups without and with psychosis.
Modeling NPI symptom-endophenotype-genotype relationships, and taking into account possible confounds (i.e. demographic characteristics, comorbidities, concomitant pharmacological treatments, and disease severity) by latent variable models, COMT and 5-HTTLPR genetic variations correlated with "frontal" and "psychosis" endophenotypes.
These findings claim for a synergic effect of COMT*H and 5-HTTLPR*S polymorphisms on the risk of psychosis in AD and for their interaction with disease stage and ischemic cardiomyopathy.
However, marginal associations were observed between the 5-HTT LPR and VNTR variants and psychosis (P < or = 0.05) indicating a minor contribution to psychosis of genetic alterations in this gene.
In the present study we investigated the original cohort of subjects to evaluate the 5-HTTLPR possible influence on the psychopathology of major psychoses in interaction with DRD4.
Patients with the 5-HTTLPR II genotype (n = 19) had significantly higher BPRS ratings for psychosis than patients with the Is (n = 25) or ss (n = 6) genotypes.