Lower serum cytokine levels in smokers than nonsmokers with chronic schizophrenia on long-term treatment with antipsychotics

Objective  Schizophrenia is associated with various abnormalities in the immune system. Suppression of inflammatory cytokines by cigarette smoke is well-established. The purpose of this study was to determine any differences in cytokine profiles in smokers and nonsmokers with schizophrenia and whether there were any relationships among altered cytokine profiles and psychopathological symptoms. Materials and methods  Serum interleukin (IL)-2, IL-6, IL-8, and tumor necrosis factor (TNF)-α levels were measured in 96 male inpatients with DSM-IV schizophrenia: 66 smokers and 30 nonsmokers. Symptoms were assessed with the Positive and Negative Syndrome Scale (PANSS). Results  The positive PANSS symptoms were lower in smokers than nonsmokers, while the negative symptoms were lower in those who smoked more cigarettes. Cytokine levels were positively correlated: IL-2 level with IL-6 and IL-6 with both IL-8 and TNF-α. Both IL-2 and IL-6, but not IL-8 or TNF-α, were significantly lower in smokers than nonsmokers (p < 0.002; p < 0.01). Lower IL-2 levels correlated with fewer negative symptoms and with smoking more cigarettes. Conclusions  The fewer positive symptoms in smokers and fewer negative symptoms in those who smoked more cigarettes may be associated with nicotine-induced suppression of some inflammatory cytokines.     

吸烟对血液过氧化与抗氧化平衡的影响

比较吸烟与不吸烟人静脉血血浆及红细胞脂质过氧化物-丙二醛（MDA）含量，血浆及红细胞超氧化物歧化酶（SOD）活力、全血谷胱甘肽过氧化物酶（GSH－Px）活力及血浆总抗氧化能力（AOA）．结果表明：吸烟组血浆及红细胞MDA的含量高于不吸烟组（P＜0．01），红细胞SOD含量高于不吸烟组（P＜0．01），血浆SOD、全血GSH－Px活力．血浆AOA均低0于不吸烟组（P＜0．01，P＜0．05，P＜0.05）．提示长期吸烟可使血中氧化与抗氧化失去平衡。     

首发精神分裂症患者脂质过氧化物及抗氧化酶水平的研究

目的：探讨氧化应激在精神分裂症发病中的作用。方法：对首发且未服药的精神分裂症患者40例,行简明精神病评定量表（BPRS）评定,并测定氧化应激相关指标。药物治疗12周后,再次进行上述检测。取40例健康志愿者外周血,检测相同生化指标。结果：患者组丙二醛（MDA）和过氧化氢酶（CAT）较对照组显著升高（P〈0.01）,而超氧化物歧化酶（SOD）及谷胱甘肽过氧化物酶（GSH-Px）显著降低（P〈0.01）。治疗后MDA和CAT较治疗前显著降低（P〈0.01）,而SOD及GSH-Px显著升高（P〈0.01）。结论：精神分裂症患者处于氧化应激状态,自由基增加,抗氧化能力降低,这些可能与精神分裂症的病理机制有关。     

Socio-demographic and clinical characteristics of heavy and non-heavy smokers among schizophrenia inpatients in a Chinese Han population

Objective

Despite higher smoking rates in schizophrenia, few studies have explored the clinical–demographic correlates of different amounts of smoking exposure. Little is known about the association between smoking severity and clinical phenotypes in Chinese patients with schizophrenia.

Materials and methods

We investigated differences between heavy (≥1 pack/day) and non-heavy (<1 pack/day) smoking in 550 male inpatients with schizophrenia using clinician-administered questionnaires and the Fagerstrom Test for Nicotine Dependence. They also were rated on the Positive and Negative Symptom Scale (PANSS), the Simpson and Angus Extrapyramidal Symptom Rating Scale (SAES), and the Abnormal Involuntary Movement Scale (AIMS), as well as were assayed with laboratory tests and an electrocardiogram.

Results

Heavy smoking prevalence was approximately 31 %. Compared to the non-heavy smokers, the heavy smokers were younger, more with paranoid subtype but less with disorganized subtype schizophrenia, smoked at an earlier age, fewer getting clozapine or all atypical antipsychotics together, and were taking larger doses of antipsychotic drugs. The heavy smokers scored significantly lower on the PANSS negative symptom subscore and total score, and also on the SAES and AIMS scores than the non-heavy smokers. In addition, heavy smokers displayed longer rate-corrected electrocardiographic QT intervals, but without any significant differences in other laboratory tests.

Conclusion

Our results suggest several clinical or demographic differences between the heavy and non-heavy smoking patients with schizophrenia in a Chinese population. Heavy smoking remains a general health risk for schizophrenia.     

Superoxide dismutase and cytokines in chronic patients with schizophrenia: association with psychopathology and response to antipsychotics

Objective  Both schizophrenia and oxidative stress have been associated with immune system abnormalities in interleukin-2 and -6 (IL-2; IL-6) and increases in superoxide dismutase (SOD) activity. These abnormalities may improve during antipsychotic drug treatment that reduces symptoms in schizophrenic patients. Materials and methods  Subjects included 30 healthy controls (HC) and 78 schizophrenic (SCH) in-patients who were randomly assigned to 12 weeks of double-blind treatment with risperidone 6 mg/day or haloperidol 20 mg/day. Ratings using the Positive and Negative Syndrome Scale (PANSS) were correlated with blood SOD and serum IL-2 levels. Results  SCH patients who were medication-free for 2 weeks had greater SOD, IL-2, and IL-6 levels than HC. At baseline, these SOD elevations were associated with higher PANSS total scores and the IL-2 elevations with lower PANSS positive symptom scores. The SOD and IL-2 levels in the SCH were also positively correlated. After treatment, PANSS positive symptoms and both SOD and IL-2 showed a significant decrease, but IL-6 showed no change. The SOD and IL-2 reductions were correlated with the reductions in PANSS total score, and SOD reductions also correlated with positive subscore reductions. Females showed these associations more strongly than males. Conclusion  Our results suggest that the dysregulation in the cytokine system and oxidative stress in patients with schizophrenia is implicated in clinical symptoms and is improved at least partially with antipsychotic treatment. The stronger associations in females deserve further study and confirmation.     

D-serine adjuvant treatment alleviates behavioural and motor symptoms in Parkinson's disease

Parkinson's disease (PD) manifestations include motor symptoms and behavioural deficits that resemble schizophrenia negative symptoms. The N-methyl-D-aspartate subtype of glutamate receptor (NMDAR) represents a novel pharmacological target in PD. D-serine (DSR) allosterically modulates in-vivo NMDAR-mediated neurotransmission and has been shown to improve negative and antipsychotic drug-induced parkinsonian symptoms in schizophrenia patients. This pilot study assessed DSR effects in ten PD patients who completed a 6-wk double-blind, placebo-controlled, crossover adjuvant treatment trial with 30 mg/kg.d DSR. Primary outcome analyses consisted of separate repeated-measures multivariate analyses of variance for Unified Parkinson's Disease Rating Scale (UPDRS), Simpson-Angus Scale for Extrapyramidal Symptoms (SAS), Abnormal Involuntary Movement Scale (AIMS), and Positive and Negative Syndrome Scale (PANSS) scores. DSR treatment was well tolerated and resulted in increased DSR serum levels (p=0.001) and significantly reduced UPDRS (p=0.02), SAS (p=0.009) and PANSS (0.05) total scores. These preliminary findings suggest that DSR treatment may be beneficial in PD. Larger-sized studies with optimized DSR dosages are warranted.     

线粒体基因突变型糖尿病患者氧化应激状态的临床研究

目的:观察线粒体基因突变型糖尿病(mitochodrial diabetes mellitus,mtDM)患者体内氧化应激状态,探讨线粒体基因突变与氧化应激的关系。方法:应用聚合酶链反应-限制性片段长度多态性法(PCR-RFLP)筛查2型糖尿病患者(T2DM组)和健康对照组(C组)mtDNA tRNALE(UUUR)3243A→G(A3243G)和mtDNAND412026A→G(A12026G)突变位点发生情况,用酶反应化学比色法测定线粒体基因突变型糖尿病组(mtDM组)、T2DM组及健康对照组外周血中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、抗活性氧活力(Anti-ROS)和丙二醛(MDA)等氧化应激指标。结果:(1)与C组相比,mtDM组和T2DM组Anti-ROS、SOD、GSH-Px、CAT活性及SOD/MDA均下降(P<0.05),MDA含量升高(P<0.05或P<0.01)。(2)mtDM组与T2DM组相比,CAT活性下降(P<0.05),MDA含量升高(P<0.05或P<0.01)。(3)A3243G突变组和A12026G突变组之间SOD、GSH-Px、CAT、Anti-ROS活性和MDA差异无统计学意义(P>0.05)。结论:线粒体基因突变型糖尿病较无突变2型糖尿病患者及健康对照组氧化应激损伤更严重,可能与线粒体基因突变有关。     

Effects of trichlorfon on malondialdehyde and antioxidant system in human erythrocytes

Organophosphorus insecticides may induce oxidative stress leading to generation of free radicals and alteration in antioxidant system. The aim of this study was to examine the potency of trichlorfon, an organophosphate insecticide, to induce oxidative stress response in human erythrocytes in vitro. For this purpose trichlorfon solutions in different concentrations and erythrocyte solutions were incubated at 37 °C for 60 min. At the end of the incubation time, malondialdehyde (MDA), an end product of lipid peroxidation, total glutathione, reduced glutathione (GSH) levels, activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzymes were determined by spectrophotometric methods. Trichlorfon increased MDA formation depended on the concentration. On the other hand, decreases in the GSH-Px activity, GSH levels and increases in the total glutathione levels, SOD and CAT activities were seen in the studied concentrations. The present findings indicate that the in vitro toxicity of trichlorfon may be associated with oxidative stress.     

中国男性精神分裂症患者吸烟、精神病理学、认知功能和治疗相关不良反应的病例对照研究(英文)

目的:美洲和欧洲的精神分裂症患者的吸烟率是社区人群对照的3至4倍,与阴性症状和锥体外系综合征的减少及认知功能的改善有关。本研究的目的是在中国精神分裂症患者中观察这些因素的临床关联性。方法:采用尼古丁依赖自评量表(Fagerstrom Test for Nicotine Dependence,FTND)和重复性成套神经心理状态测验(Repeatable Battery for the Assessment of Neuropsychological Status,RBANS),我们对776例男性和560例男性社区对照进行了比较。患者也测评了阳性和阴性症状量表(Positive and Negative Symptom Scale,PANSS)、Simpson -Angus锥体外系副反应评定量表(Simpson and Angus Extrapyramidal Symptom Rating Scale,SAES)和不自主运动量表(Abnormal Involuntary Movement Scale,AIMS)。结果:精神分裂症患者终生吸烟率较社区对照人群高(79%比63%),同时严重吸烟者与对照组之间有更明显的差异(61%比31%)。现在吸烟者的PANSS阴性症状和SAES帕金森综合征得分均低于非吸烟者。吸烟的精神分裂症患者在RBANS认知功能测试中表现最差,非吸烟精神分裂症患者较差,之后是吸烟者,非吸烟者对照表现最好。结论:中国精神分裂症患者的吸烟率高于社区对照人群,但精神分裂症患者和对照组之间尼古丁依赖率与美洲观察到的情况有很大的差异。吸烟与较低水平的阴性症状,较少的锥体外系综合征及较少的帕金森综合征相关联,提示自我治疗的存在。但是,吸烟在精神分裂症患者和对照组人群中都与显著的认知功能损害相关联。     

葛根素在减轻创伤性脑损伤氧化应激反应中的作用

目的：探究葛根素是否能有效减轻创伤性脑损伤（TBI）中的氧化应激反应。方法选择成年雄性 SD大鼠60只构建 TBI 模型并随机平分为模型组,假手术组及葛根素给药组（给药组）,每组20只。检测3组大鼠在不同时间点氧化应激相关指标[超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH－Px）、过氧化氢酶（CAT）、丙二醛（MDA）]活性及含量变化。结果氧化应激相关指标检测中,给药组与模型组比较,其中第3、7天 SOD、CAT 活性以及 MDA、NO 含量与同时间点模型组比较差异有统计学意义（ P ＜0．05）。用药组与模型组比较,均能不同程度升高GSH 含量及 GSH－Px 活性（ P ＜0．05）,其中给药组第3天及第7天 GSH 含量及 GSH－Px 活性较同时间点模型组比较差异有统计学意义（ P ＜0．05）。结论根据对不同氧化应激指标检测所得结果可以看出葛根素可有效减轻创伤性脑损伤所带来的氧化应激损伤。     

Toxicity and oxidative stress induced by T-2 toxin in cultured mouse Leydig cells

To explore the toxic mechanism of T-2 toxin on Leydig cells of mice, we would investigate the toxicity and oxidative stress induced by T-2 toxin in the cells. Leydig cells were isolated and cultured with control or T-2 toxin (10^?7 M, 10^?8 M, or 10^?9 M) for 24?h, then cells and supernatants were harvested to examine cell viability, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities, expression of messenger RNA (mRNA) related to oxidative stress, malondialdehyde (MDA) content and DNA damage. The cell viability was evaluated in mouse Leydig cells by MTT assay, MDA content and SOD, GSH-Px and CAT activities were measured by routine kits, expression of mRNA related to oxidative stress were examined by quantitative real-time polymerase chain reaction (PCR), and DNA damage was investigated by comet assay. Leydig cells treated with T-2 toxin showed significant reductions in cell viability, SOD, GSH-Px and CAT activities, and expression of mRNA related to oxidative stress, and remarkable increases in MDA content and levels of DNA damage. This study proves that T-2 toxin is toxic to Leydig cells of mice. Furthermore, oxidative stress plays an important role in the above-mentioned negative effects of T-2 toxin.     

参麦注射液治疗急性ST段抬高型心肌梗死合并心源性休克的疗效及机制研究

目的:探讨参麦注射液治疗急性ST段抬高型心肌梗死(STEMI)合并心源性休克(CS)的疗效及机制。方法:将STEMI合并CS(STEMI+CS)患者112例随机分为2组,即对照组和实验组,每组各56例。对照组患者实施常规治疗方案,实验组患者实施常规治疗联合参麦注射液治疗方案。观察2组患者治疗前后心功能评价指标,包括平均动脉压(MAP)、心排血量(CO)、左室射血分数(LVEF)、心脏指数(CI)、每搏输出量(SV)和心率(HR),血清心肌损伤标志物,包括乳酸脱氢酶(LDH)、肌酸激酶同工酶(CK-MB)、天门冬氨酸氨基转移酶(AST)、肌红蛋白(MYO)和心肌肌钙蛋白I(cTNI)以及血清氧化应激参数,包括丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)和超氧化物歧化酶(SOD)。结果:与治疗前相比,对照组和实验组患者分别经2种治疗方案治疗后心功能评价指标MAP、CO、LVEF、CI和SV均显著增加(P<0.01),HR均显著降低(P<0.01),血清心肌损伤标志物LDH、CK-MB、AST、MYO和cTNI均显著降低(P<0.01)。与对照组治疗后相比,实验组治疗后MAP、CO、LVEF、CI和SV分别增加了15%、7%、12%、12%和9%(P<0.01),HR降低了5%(P<0.01),血清LDH、CK-MB、AST、MYO和cTNI分别降低了9%、42%、28%、34%和25%(P<0.01),实验组治疗后效果要明显优于对照组治疗后效果。氧化应激参数结果显示,与对照组治疗前相比,对照组治疗后血清MDA、GSH-Px、CAT和SOD的含量无明显变化(P>0.05);与实验组治疗前相比,实验组治疗后血清MDA含量显著降低(P<0.01),GSH-Px、CAT和SOD含量显著增加(P<0.01)。与对照组治疗后相比,实验组治疗后MDA降低了47%(P<0.01),GSH-Px、CAT和SOD分别增加了26%、42%和29%(P<0.01)。结论:参麦注射液能够改善STEMI+CS患者的心功能,降低血清心肌损伤标志物以及改善血清氧化应激参数,其效果明显优于常规治疗效果,参麦注射液改善STEMI+CS患者临床疗效的作用机制可能与其降低患者体内氧化应激水平有关。     

硒化卡拉胶联合表阿霉素对H22肝癌小鼠抗氧化作用的研究

目的 通过体内抗肿瘤试验,研究硒化卡拉胶联合表阿霉素对H22肝癌移植瘤生长的抑制及抗氧化作用。方法 将H22移植性肝癌小鼠随机分为8组,每组10只,治疗期间考察各组小鼠的体重变化及生存状态。停药次日,对脾指数、胸腺指数、抑瘤率进行测定,并检测血清中GSH-Px、SOD、CAT活性及GSH、MDA的含量变化。结果 KSC单独及联合EPI可改善H22小鼠的免疫器官指数,提高抑瘤率;与模型对照组相比,中、高剂量KSC可显著提高GSH-Px、CAT活性及GSH含量(P<0.05),高剂量KSC可显著提高SOD活性(P<0.01),同时各EPI组GSH-Px、SOD、CAT活性均显著降低(P<0.05),而MDA显著增高(P<0.01);中、高剂量KSC联合EPI可使GSH-Px、SOD、CAT活性均显著恢复(P<0.05),而MDA含量显著降低(P<0.01)。结论 硒化卡拉胶具有良好的免疫调节和抗氧化作用,联合用药可显著改善表阿霉素的毒副作用,提高机体抗氧化水平,对治疗小鼠移植性肝癌有显著的增效作用。     

冠心汤治疗前后冠心病病人血液过氧化反应及红细胞变形性的变化

为研究冠心汤对冠心病患者血液过氧化反应及红细胞变形性的影响，我们检测了冠心病患者使用冠心汤治疗前后红细胞SOD，全血GSH－PX、CAT活力，血浆AOA和红细胞膜MDA含量及IF的变化，结果表明，冠心病患者SOD、GSH－Px、CAT活力及AOA明显低于对照组（H＜0．01），MDA含量及IF明显高于对照组（P＜0．01）。治疗后，SOD、GSHPx、CAT活力明显高于治疗前（P＜0．05），MDA含和IF明显低于治疗前（P＜0．05，P＜0．01）。提示冠心汤能降低冠心病患者血液的过氧化反应，提高红细胞变形能力。     

The influence of the CYP2D6 polymorphism on psychopathological and extrapyramidal symptoms in the patients on long-term antipsychotic treatment

Poor response to antipsychotics treatment and extrapyramidal side effects (EPS) are the most challenging problems in the treatment of schizophrenia. Several studies were investigating the impact of polymorphic cytochrome P450 2D6 gene (CYP2D6) on EPS but the results were conflicting. There are practically no clinical studies of long-term treatment of schizophrenia and CYP2D6 polymorphism. Our aim was to evaluate the influence of CYP2D6 genotype on psychopathological symptoms and the occurrence of EPS in Slovenian outpatients with schizophrenia or schizoaffective disorder in stable remission, receiving long-term maintenance antipsychotic treatment. In total 131 outpatients meeting the DSM IV criteria for schizophrenia or schizoaffective disorder and receiving maintenance therapy with haloperidol, fluphenazine, zuclopethixole or risperidone were genotyped for 14 polymorphic CYP2D6 alleles. Psychopathological symptoms were assessed with the Positive and Negative Symptom Scale for Schizophrenia (PANSS). EPS were assessed with the Simpson Angus Scale (SAS), the Barnes Akathisia Scale and the Abnormal Involuntary Movement Scale (AIMS). Six patients (4.6%) were genotyped as poor metabolizers (PMs). PMs scored significantly higher on the negative subscale for PANSS. There were no statistically significant differences between the group of PMs and the group of patients with at least one functional CYP2D6 allele in view of patient's characteristics or any of the items of the AIMS, the SAS or the Barnes Akathisia Scale. CYP2D6 genotype may not be the major factor that determines the susceptibility to antipsychotic-induced EPS in Slovenian patients in stable remission and on maintenance therapy with antipsychotics that are mainly CYP2D6 substrates. However, CYP2D6 genotype might be a factor contributing to the persistent negative symptoms of schizophrenia.     

Effects of cigarette smoking on psychopathology scores in patients with schizophrenia: An experimental study

Cigarette smoking and/or nicotine administration have been shown to transiently ameliorate several psychophysiological deficits in patients with schizophrenia such as indicators of deficient sensory gating and attention, but acute effects of smoking on positive and negative symptoms in schizophrenia have not been evaluated in experimental paradigms. The current study assessed whether smoking of cigarettes, after 6–12 h abstinence, transiently alters the expression of negative and/or positive symptoms in patients with schizophrenia who have a history of regular smoking. In a double‐blind, placebo controlled study patients with schizophrenia participated in two sessions in which they smoked either cigarettes moderately high in nicotine content or denicotinized cigarettes. They were interviewed pre‐and postsmoking to obtain ratings of PANSS and SANS scales, and had blood pressure and pulse serially recorded before and after smoking. Pulse rate and blood pressure were slightly higher after smoking in the high nicotine cigarette session. Negative symptom scores on both scales were significantly lower after cigarette smoking compared to same‐day predrug baseline, but there were no differences in active versus denicotinized cigarette drug effects. These results suggest that acute smoking of cigarettes reduces negative symptoms in patients with schizophrenia in this experimental paradigm. Future work needs to identify the mechanism responsible for this behavioral effect.     

Effects of Cigarette Smoking on Psychopathology Scores in Patients With Schizophrenia: An Experimental Study

Cigarette smoking and/or nicotine administration have been shown to transiently ameliorate several psychophysiological deficits in patients with schizophrenia such as indicators of deficient sensory gating and attention, but acute effects of smoking on positive and negative symptoms in schizophrenia have not been evaluated in experimental paradigms. The current study assessed whether smoking of cigarettes, after 6–12 h abstinence, transiently alters the expression of negative and/or positive symptoms in patients with schizophrenia who have a history of regular smoking. In a double-blind, placebo controlled study patients with schizophrenia participated in two sessions in which they smoked either cigarettes moderately high in nicotine content or denicotinized cigarettes. They were interviewed pre-and postsmoking to obtain ratings of PANSS and SANS scales, and had blood pressure and pulse serially recorded before and after smoking. Pulse rate and blood pressure were slightly higher after smoking in the high nicotine cigarette session. Negative symptom scores on both scales were significantly lower after cigarette smoking compared to same-day predrug baseline, but there were no differences in active versus denicotinized cigarette drug effects. These results suggest that acute smoking of cigarettes reduces negative symptoms in patients with schizophrenia in this experimental paradigm. Future work needs to identify the mechanism responsible for this behavioral effect.     

Role of reactive oxygen species in organophosphate insecticide phosalone toxicity in erythrocytes in vitro.

Reactive oxygen species (ROS) caused by organophosphates may be involved in the toxicity of various pesticides. Therefore, in this study we aimed to investigate how an organophosphate insecticide, phosalone, affects lipid peroxidation (LPO) and the antioxidant defence system in vitro. For this purpose, the effects of various doses of phosalone on LPO and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) in erythrocytes were studied. Each phosalone dose was incubated with a previously prepared erythrocyte sample at +4 degrees C for 0, 60 and 180 min. After incubation, the levels of malondialdehyde (MDA) and the activities of SOD, GSH-Px and CAT were determined. Phosalone caused an increase in MDA formation and a decrease in the activities of SOD, GSH-Px and CAT. However, these effects were seen only at extremely high concentrations of phosalone and these concentrations were in the lethal range. Therefore, we suggest that ROS may not involve in the toxic effects of the pesticidal use of phosalone in low concentrations.     

Clinical utility of the Negative Symptom Assessment-16 in individuals with schizophrenia

This study examined the clinical utility of the Negative Symptom Assessment-16 (NSA-16) in schizophrenia. 274 individuals with schizophrenia were assessed on the NSA-16, Positive and Negative Syndrome Scale (PANSS), Clinical Assessment for Negative Symptoms (CAINS), Calgary Depression Scale for Schizophrenia (CDSS), Social and Occupational Functioning Assessment Scale (SOFAS) and the Simpson-Angus Extrapyramidal Side Effects Scale (SAS). Factor analyses were conducted and Cronbach's alpha was computed. Correlations were assessed using Spearman's correlation coefficient. The 5-factor model of the NSA-16 did not give good fit statistics from our sample. Exploratory factor analysis on a randomly selected split-half of the sample followed by confirmatory factor analysis on the remaining sample supported a 4-factor structure with 12 items. The factors were: Restricted speech, Poor quality of speech, Affective blunting and Amotivation. The NSA-16 with the 12 items was termed as the NSA-12. The NSA-12 showed good internal reliability. The NSA-12 total score and global negative symptom rating had strong correlations with CAINS total and PANSS negative factor scores, suggesting good convergent validity. Weak correlations of the NSA-12 total score and global negative symptom rating with PANSS positive, CDSS and SAS scores suggested good divergent validity. The NSA-12 total score and global negative symptom rating were strongly and inversely associated with SOFAS and positively associated with NSA-12 global level of functioning. In conclusion, the NSA-12 is useful to evaluate negative symptoms in clinical and research settings in individuals with schizophrenia. Our study results also support a 4-factor structure of the NSA-12 in outpatients with schizophrenia.