This two years long prospective longitudinal study with all HYFEPA (n = 42) admitted to EQIIP SOL between 2012-2015 reports at multiple time points, clinical (CGI, GAF), functional (SOFAS, work/study, housing autonomy) and substance use disorder (DUS, AUS) outcomes and acute services use (hospitalizations, emergency room visits).
In order to test this hypothesis, we examined fasting, morning plasma concentrations of beta-endorphin and two catecholamine metabolites in prepubertal boys naive to drugs of abuse and at elevated familial risk for a substance use disorder (SA+), and in controls (SA-).
Single and multiple marker analyses revealed association between two SNPs located at the 3' region of miR-96 (rs2402959 and rs6965643) and ADHD without SUD.
They showed lower traits of the SWAP-200's cluster A and B disorders than SUD and PD patients, who presented more severe levels of personality impairment.
An association of genotype distribution and allele frequency of the 5-HTR1A C(-1019)G locus was observed in schizophrenia (chi2=9.51, d.f.=2, p=0.009; chi2=9.52, d.f.=1, p=0.002; Armitage's trend test: chi2=9.07, d.f.=1, p=0.003), in substance use disorder (chi2=8.41, d.f.=2, p=0.015; chi2=8.35, d.f.=1, p=0.004; Armitage's trend test: chi2=6.27, d.f.=1, p=0.0012), and in panic attack (chi2=6.31, d.f.=2, p=0.043; chi2=6.14, d.f.=1, p=0.013; Armitage's trend test: chi2=6.27, d.f.=1, p=0.012).
By means of Physical Activity Rating Scale (PARS-3), internal Inhibition Scale and Drug Craving Scale, this study investigated the individuals with substance use disorder under rehabilitation in the women compulsory isolation rehabilitation center in Chongqing, China.
Our results provide preliminary evidence for the contribution of two sequence variants at the miR-183-96-182 cluster to ADHD without comorbid SUD, and emphasize the need to take comorbidities into account in genetic studies to minimize the effect of heterogeneity and to clarify these complex phenotypes.
We examined the association of CTF score with risk for psychiatric and substance use disorders in these samples and the OZ-ALC GWAS sample (N = 1538) in which CT Study factor loadings were applied.
Repeated measurements of anxiety sensitivity and coping motives throughout treatment were examined from a randomized clinical trial comparing usual, CBT-based treatment at a substance use disorder specialty clinic (UC) to that usual care plus a brief CBT for anxiety program for patients with comorbid anxiety and substance use disorders (CALM ARC).
Building on the work of others, we suggest individual risk for SUD emerges from an immature PFC combined with hyper-reactivity of reward salience, habit, and stress systems.
Compared to controls, ADHD patients (with and without SUDs) showed significantly increased frequency of the DBH (rs2519152: OR 1.73; CI 1.15-2.59; P=0.008) and the OPRM1 risk genotypes (rs1799971: OR 1.71; CI 1.17-2.50; P=0.006).
They showed lower traits of the SWAP-200's cluster A and B disorders than SUD and PD patients, who presented more severe levels of personality impairment.
Indeed a variety of rodent models for schizophrenia display behavioral and physiological features relevant to SUD including: neurodevelopmental models, models of a rare variant (Disc1), to models of common variants (neurexin, dysbindin and neuregulin), and models of various gene-drug interactions.
Indeed a variety of rodent models for schizophrenia display behavioral and physiological features relevant to SUD including: neurodevelopmental models, models of a rare variant (Disc1), to models of common variants (neurexin, dysbindin and neuregulin), and models of various gene-drug interactions.
Imaging gene-substance interactions: the effect of the DRD2 TaqIA polymorphism and the dopamine agonist bromocriptine on the brain activation during the anticipation of reward.
We found three candidate genes associated with both BD and TUD (COMT, SLC6A3, and SLC6A4) and commonality analysis suggests that these genes interact in predisposing psychiatric and substance use disorders.
The results represent the first evidence in humans that the CNR1 gene is a risk factor for depression--and probably also for co-morbid psychiatric conditions such as substance use disorders--through a high neuroticism and low agreeableness phenotype.
As evidence continues to accumulate, neutral CB1R antagonists (such as AM4113), CB2R agonists (JWH133, Xie2-64), and nonselective phytocannabinoids (cannabidiol, β-caryophyllene, ∆<sup>9</sup>-tetrahydrocannabivarin) have shown great therapeutic potential for SUDs, as shown in experimental animals.