OBJECTIVES: The aim of the present study was to evaluate the relationship of borderline personality features (BPFs) with attention-deficit/hyperactivity disorder (ADHD) symptoms among male patients with substance use disorder (SUD) and to evaluate the impact of emotion dysregulation on this relationship. We also wanted to control the effects of depression and state anxiety. METHOD: Participants included 305 treatment-seeking male patients with SUD. Participants were evaluated by applying the Borderline Personality Inventory (BPI), the Adult ADHD Self-Report Scale (ASRS), the Difficulties in Emotion Regulation Scale (DERS) and the Beck Depression Inventory (BDI), and the Spielberger State-Trait Anxiety Inventory (STAI). RESULTS: Age, duration of education, marital status, employment status, age at first and age at regular substance use did not differ between those with probable borderline personality disorder (BPD) (n = 155, 50.8%) and those without probable BPD (n = 150, 49.2%). Probable ADHD risk was 3.5 times higher among those with probable BPD. Also ADHD, DERS, depression and anxiety scores were higher in this group with probable BPD. Scale scores were mild and moderately correlated with each other. In hierarchical regression analysis severity of ADHD symptoms (particularly hyperactivity/impulsivity [HI] dimension), together with difficulties in emotion regulation (particularly impulse control difficulties), depression and trait anxiety predicted the severity of BPFs. CONCLUSIONS: These findings suggest that the severity of HI symptoms of ADHD is related with the BPFs, while difficulties in emotion regulation, particularly impulse control difficulties, partially mediate this relationship among patients with SUD.
Schizophrenia (SZ) is a mental disorder with a strong genetic basis as well as epigenetic aspects. Siblings of patients with SZ can share certain endophenotypes with the patients, suggesting that the siblings may be important for distinguishing between trait and state markers. In the current study, we aimed to characterize the balance between pro-BDNF/mature BDNF and its receptors p75NTR/TrkB, which is tpa-BDNF pathways proteins and thought to play a role in synaptic pruning as a possible endophenotype of schizophrenia. Forty drug-naïve patients with rst-episode psychosis (FEP) matched for age, gender and level of education, 40 unaffected siblings (UAS) of patients with FEP and 67 healthy controls (HC) were included in the study. Blood samples were collected from all participants to determine BDNF, pro-BDNF, TrkB and p75NTR, PAI1, tPA, ACTH and cortisol levels. We showed that levels of proteins of the tPA-BDNF pathway, pro-BDNF/m-BDNF and p75NTR/TrkB ratios could successfully differentiateFEP and their siblings from the HCs by using ROC analysis. Plasma levels of m-BDNF were found to be the lowest in the healthy siblings and highest in the healthy control group with statistically signi cant differences between all 3 groups. The plasma levels of pro-BDNF in the healthy control group were similar to the FEP patients, the same in the healthy siblings of the FEP patients. Our data Support the hypothesis that imbalance between neurotrophic and apoptotic proteins might occur in SZ, and this imbalance could be an endophenotype of the disease.
Schizophrenia (SZ) is a mental disorder with a strong genetic basis as well as epigenetic aspects. Siblings of patients with SZ can share certain endophenotypes with the patients, suggesting that the siblings may be important for distinguishing between trait and state markers. In the current study, we aimed to characterize the balance between pro-BDNF/mature BDNF and its receptors p75NTR/TrkB, which is tpa-BDNF pathways proteins and thought to play a role in synaptic pruning as a possible endophenotype of schizophrenia. Forty drug-naïve patients with first-episode psychosis (FEP) matched for age, gender and level of education, 40 unaffected siblings (UAS) of patients with FEP and 67 healthy controls (HC) were included in the study. Blood samples were collected from all participants to determine BDNF, pro-BDNF, TrkB and p75NTR, PAI1, tPA, ACTH and cortisol levels. We showed that levels of proteins of the tPA-BDNF pathway, pro-BDNF/m-BDNF and p75NTR/TrkB ratios could successfully differentiateFEP and their siblings from the HCs by using ROC analysis. Plasma levels of m-BDNF were found to be the lowest in the healthy siblings and highest in the healthy control group with statistically significant differences between all 3 groups. The plasma levels of pro-BDNF in the healthy control group were similar to the FEP patients, the same in the healthy siblings of the FEP patients. Our data Support the hypothesis that imbalance between neurotrophic and apoptotic proteins might occur in SZ, and this imbalance could be an endophenotype of the disease.
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