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This study aimed to investigate whether 12-week moderate-intensity aerobic exercise has beneficial effects on oxidative stress markers in blood and on cognitive functions in patients who have methamphetamine dependence. Serum levels of oxidative stress markers, including total anti-oxidation capability, super oxide dismutase (SOD), catalase (CAT), and methane dicarboxylic aldehyde (MDA), were measured at baseline (all participants) and the 12-week follow-up (methamphetamine-dependent patients). Serum levels of CAT and MDA in methamphetamine-dependent patients ( n  = 68) were higher than those in healthy controls ( n  = 35) at baseline. Furthermore, the international shopping list (ISL) task scores of methamphetamine-dependent patients were significantly lower than those of the controls, indicating verbal memory deficits in methamphetamine-dependent patients. Although there were no significant interactions for all cognitive function scores, aerobic exercise improved the processing speed in methamphetamine-dependent patients. Of interest, aerobic exercise significantly attenuated a spontaneous increase in serum MDA levels in methamphetamine-dependent patients after 12-weeks of abstinence. In conclusion, this study showed that methamphetamine-dependent patients with verbal learning and memory deficits have higher serum levels of MDA, and that a 12-week aerobic exercise program may have beneficial effects on the processing speed as well as blood lipid peroxidation in methamphetamine-dependent patients. [ABSTRACT FROM AUTHOR]

• There is a significant shared genetic basis between SCZ and cigarette and cannabis smoking (SCZ_SMO) which consisted of 8.6% of SCZ heritability. • At the significance threshold of p <5 × 10−8, 20 loci were significantly associated with SCZ_SMO, which had a heritability of 0.03. • Brain expression level of NCAM1, as well as other genes involved in neuron and dendritic spinal head, was positively associated with SCZ_SMO. • SCZ_SMO has a positive genetic association with both reverse mental and physical conditions, such as social deprivation, lifestyle problems, pregnancy loss, ADHD, etc. Confirming the existence and composition of the shared genetic basis of Schizophrenia and cannabis and cigarette smoking has critical values for the clinical prevention and intervention of psychosis. To achieve this goal, we leveraged Genome-Wide summary statistics of Schizophrenia (n = 99,934), cigarette smoking (n = 518,633) and cannabis usage (n = 162,082). We applied Causal Analysis Using Summary Effect Estimates (CAUSE) and genomic structural equation modeling (GenomicSEM) to quantify the contribution of a common genetic factor of cannabis and cigarette smoking and schizophrenia (referred to as SCZ_SMO), then identified genome-wide loci that made up SCZ_SMO. We estimated that SCZ_SMO explained 8.6% of Schizophrenia heritability (Z score <-2.5 in CAUSE, p <10−20 in Genomic SEM). There were 20 independent loci showing association with SCZ_SMO at the genome-wide threshold of p <5 × 10−8. At the top locus on chromosome 11, fine-mapping identified rs7945073 (posterior inclusion probability =0.12, p = 2.24 × 10−32) as the top risk variants. Gene-level association and fine-mapping highlighted NCAM1, PHC2, and SEMA6D as risk genes of SCZ_SMO. Other risk genes were enriched in cortex, neuron, and dendritic spines (adjusted p <0.05). SCZ_SMO showed significant positive correlation (p <10−6) with the genetic risk of attention deficit hyperactivity disorder (r = 0.50), lifestyle problems (r = 0.83), social deprivation (r = 0.58) and all-cause pregnant loss (r = 0.60). Our result provided new evidence on the shared genetic basis model for the association between Schizophrenia and smoking and provided genetic and biological insights into their shared mechanism. [ABSTRACT FROM AUTHOR]

Abstract: This case–control study enrolled 578 obsessive–compulsive disorder (OCD) patients and 649 controls and genotyped rs10491734, rs2228622, rs301430 and rs301443 to replicate association of the SLC1A1 gene with OCD in ethnic Han Chinese. The G-A-C-G and G-G-T-C haplotypes were found to be significantly associated with OCD in overall samples, male samples and female samples. [Copyright &y& Elsevier]

Autism is a neurodevelopmental disorder characterized by abnormal reciprocal social interactions, communication deficits and repetitive behaviors with restricted interests. A previous quantitative proteomic profiling study demonstrated that microtubule-associated stable tubule only polypeptide (STOP; also known as MAP6) protein was significant reduced in the cerebral cortex from BTBR mouse model of autism compared to the C57BL/6J mice. In the present study, the result showed that the concentration of STOP/MAP6 protein was significantly reduced in the plasma of autistic subjects than that in healthy controls. Finally, a possible mechanism of STOP/MAP6 protein in the pathogenesis of autism was proposed. [ABSTRACT FROM AUTHOR]

Abstract: Decreased dopaminergic activity in the prefrontal cortex (PFC) has been consistently reported in schizophrenia patients. The dopamine D1 receptor (DRD1) plays an important role in mediating dopaminergic transmission in the PFC. Controversy about this topic still exists despite ample evidence suggesting that the DRD1 gene is associated with performance on neuropsychological tests probing the function of the PFC in schizophrenia, as well as positive and negative symptoms and therapeutic response to antipsychotics. To determine whether this gene is involved in the etiology of schizophrenia, we undertook a case–control study to look for an association. We genotyped five single nucleotide polymorphisms (SNPs) rs4532, rs5326, rs2168631, rs6882300 and rs267418 within the DRD1 involving 373 schizophrenia patients with early age of onset and 379 healthy subjects. No significant differences of genotype, allele or haplotype distribution were identified between patients and controls. Our results do not preclude a possible role of DRD1 in the etiology of schizophrenia. As an important dopaminergic gene, DRD1 may contribute to schizophrenia by interacting with other genes. Further relevant studies are warranted. [Copyright &y& Elsevier]

Abstract: In this study, we analyzed four single nucleotide polymorphisms (SNPs) (rs10491734, rs2228622, rs301430 and rs301443) of the solute carrier family 1 gene (SLC1A1) in a set of 616 schizophrenia patients and 638 matched healthy controls of Han Chinese descent. No significant differences of genotype or allele distribution were identified between the patients and controls. Our data suggest that SLC1A1 is unlikely to be a major susceptibility gene for schizophrenia in Han Chinese. [Copyright &y& Elsevier]