| 1 | Amyloid 2000 Jun 7: 105-10 |
|---|---|
| PMID | 10842712 |
| Title | Serum amyloid A in Alzheimer's disease brain is predominantly localized to myelin sheaths and axonal membrane. |
| Abstract | Immunohistochemical localization of the injury specific apolipoprotein, acute phase serum amyloid A (A-apoSAA), was compared in brains of patients with neuropathologically confirmed Alzheimer's disease (AD), multiple sclerosis (MS), Parkinson's disease (PD); Pick's disease (Pick's), dementia with Lewy bodies (DLB), coronary artery disease (CAD), and schizophrenia. Affected regions of both AD and MS brains showed intense staining for A-apoSAA in comparison to an unaffected region and non-AD/MS brains. The major site of A-apoSAA staining in both diseases was the myelin sheaths of axons in layers V and VI of affected cortex. A-apoSAA contains a cholesterol binding site near its amino terminus and is likely to have a high affinity for cholesterol-rich myelin. These findings, along with our recent evidence that A-apoSAA can inhibit lipid synthesis in vascular smooth muscle cells suggest that A-apoSAA plays a role in the neuronal loss and white matter damage occurring in AD and MS. |
| SCZ Keywords | schizophrenia |
| 2 | Neuropsychopharmacol Hung 2006 Dec 8: 201-9 |
| PMID | 17211055 |
| Title | [Switching patients with schizophrenia to ziprasidone from conventional or other atypical antipsychotics]. |
| Abstract | The aim of the study was to assess the efficacy, tolerability and safety of ziprasidone in patients with schizophrenia who were already treated with conventional or other atypical antipsychotics that had to be switched due the lack of efficacy or bad tolerance. The study was a 12-week, open label, multicenter, non comparative trial on oral ziprasidone. 106 patients with DSM-IV schizophrenia were switched to ziprasidone from their previous antipsychotic without a washout phase. The study required fixed dosing with ziprasidone. For the first week the patient received 80 mg of study drug daily, followed for 3 weeks 120 mg/day. Subsequently for 8 weeks either 80 mg, or 120 mg, or 160 mg total daily dose could be given at the discretion of the investigator. Baseline and outcome assessment included Positive and Negative Syndrome Scale (PANSS), Clinical Global Impression Severity of Illness Subscale (CGI-S) and Global Improvement Subscale (CGI-I), Calgary Depression Scale (CAD), Hamilton Depression Scale (HAMD), Drug Attitude Inventory (DAI), Simpson Angus Extrapyramidal Symptoms Rating Scale (SAS) and Barnes Akathisia Rating Scale (BARS). Changes in overall body weight were also evaluated. After 12 weeks on ziprasidone therapy, significant improvements were observed on all major symptoms measures and subscales. 34 (51,5%) patients (ITT) were rated much or very much improved on CGI-I at week 12. The mean SAS score significantly reduced during the ziprasidone treatment period (p<0.001). In the DAI ziprasidone treatment was also favorable rated. During treatment with ziprasidone for 12 weeks the body weight of the patients was significantly reduced (mean: 1,2 kg, SD=3,79, p=0.002). 58 adverse events occurred in 41 subjects (38.7%), of whom 7 patients (6.6%) encountered 9 severe adverse events. The adverse events were mainly mild and moderate. 15 patients (14.2%) were discontinued from the study due to adverse events. The reason for discontinuation in 4 cases was mainly insufficient clinical response. Switching patients from their previous antipsychotic to ziprasidone without a washout phase was generally well tolerated and was associated with symptoms improvements 12 weeks later. At least 50% of patients who needed to be switched because of unsatisfactory efficacy or poor tolerance were significantly improved on ziprasidone therapy. The favorable safety profile of ziprasidone treatment was consistent with that seen in other clinical trials. switching, ziprasidone, schizophrenia. |
| SCZ Keywords | schizophrenia |
| 3 | Klin Med (Mosk) 2007 -1 85: 33-6 |
| PMID | 17564035 |
| Title | [The clinical features of the course of coronary artery disease in patients with schizophrenia]. |
| Abstract | Thirty-nine patients suffering from coronary artery disease (CAD) and schizophrenia (main group) and 32 mentally healthy CAD patients (control group) were included in the study. Cardiological examination including complaint and anamnesis analysis, ECG, EchoCG, stress-EchoCG with dobutamine, 24-hour Holter ECG monitoring was performed; coronaroangiography was carried out in 15 patients. Acute circulatory insufficiency, early post-infarction stenocardia, and chronic left ventricular aneurism were found to be more frequent in patients with schizophrenia vs. controls. Certain differences in CAD risk factors between the groups were revealed. Hyperlipidemia and type 2 diabetes were found in 14 (36%) and 1 (3%) patients in the main group vs. 20 (62%) and 6 (19%) patients in the control group (p = 0.03; p = 0.04), respectively. Glucose intolerance was found in no schizophrenia patients, while it was revealed in 5 (16%) controls (p = 0.02). Patients with schizophrenia sought medical aid later than controls. The number of main group patients who sought medical aid during the first hour, the first 4 hours, the first 4 to 12 hours, or the first 12 to 24 hours was 2 (3%), 3 (5%), 16 (27%), and 38 (64%), respectively; in the control groups these numbers were 12 (30%), 21 (54%), 3 (8%), and 3 (8%), respectively (p < 0.001, p < 0.001, p = 0.02, p < 0.001, respectively). |
| SCZ Keywords | schizophrenia |
| 4 | Neurosci. Res. 2008 Feb 60: 184-91 |
| PMID | 18068248 |
| Title | Gene expression profiling of major depression and suicide in the prefrontal cortex of postmortem brains. |
| Abstract | Genome-wide gene expression analysis using DNA microarray has a great advantage to identify the genes or specific molecular casCADes involved in mental diseases, including major depression and suicide. In the present study, we conducted DNA microarray analysis of major depression using postmortem prefrontal cortices. The gene expression patterns were compared between the controls and subjects with major depression. As a result, 99 genes were listed as the differentially expressed genes in major depression, of which several genes such as FGFR1, NCAM1, and CAMK2A were of interest. Gene ontology analysis suggested an overrepresentation of genes implicated in the downregulation or inhibition of cell proliferation. The present results may support the hypothesis that major depression is associated with impaired cellular proliferation and plasticity. Comparison between the controls and suicide victims with major depression, bipolar disorder, or schizophrenia was also conducted in the present study. Two genes, CAD and ATP1A3, were differentially expressed in the three comparisons in the same direction. Interestingly, these two genes were also included in the differentially expressed 99 genes in major depression. It may be worth investigating the genes in relation to suicide or major depression. |
| SCZ Keywords | schizophrenia |
| 5 | Biol. Psychiatry 2012 Oct 72: 637-44 |
| PMID | 22520967 |
| Title | Linkage analysis followed by association show NRG1 associated with cannabis dependence in African Americans. |
| Abstract | A genetic contribution to cannabis dependence (CAD) has been established but susceptibility genes for CAD remain largely unknown. We employed a multistage design to identify genetic variants underlying CAD. We first performed a genome-wide linkage scan for CAD in 384 African American (AA) and 354 European American families ascertained for genetic studies of cocaine and opioid dependence. We then conducted association analysis under the linkage peak, first using data from a genome-wide association study from the Study of Addiction: Genetics and Environment, followed by replication studies of prioritized single nucleotide polymorphisms (SNPs) in independent samples. We identified the strongest linkage evidence with CAD (logarithm of odds = 2.9) on chromosome 8p21.1 in AAs. In the association analysis of the Study of Addiction: Genetics and Environment sample under the linkage peak, we identified one SNP (rs17664708) associated with CAD in both AAs (odds ratio [OR] = 2.93, p = .0022) and European Americans (OR = 1.38, p = .02). This SNP, located at NRG1, a susceptibility gene for schizophrenia, was prioritized for further study. We replicated the association of rs17664708 with CAD in an independent AAs sample (OR = 2.81, p = .0068). The joint analysis of the two AA samples demonstrated highly significant association between rs17664708 and CAD with adjustment for either global (p = .00044) or local ancestry (p = .00075). Our study shows that NRG1 is probably a susceptibility gene for CAD, based on convergent evidence of linkage and replicated associations in two independent AA samples. |
| SCZ Keywords | schizophrenia |
| 6 | Kaohsiung J. Med. Sci. 2014 Nov 30: 579-86 |
| PMID | 25458049 |
| Title | The metabolic syndrome and risk of coronary artery disease in patients with chronic schizophrenia or schizoaffective disorder in a chronic mental institute. |
| Abstract | The prevalence rate of metabolic syndrome (MS) and coronary artery disease (CAD) has been found to be high in patients with chronic schizophrenia. Current evidence shows that CAD is underdiagnosed in this group. Our study evaluated the prevalence of MS and the risk of CAD in patients with chronic schizophrenia in a chronic care mental hospital in southern Taiwan. We included all patients with the diagnosis of schizophrenia or schizoaffective disorder. We collected all laboratory, physical examination, psychiatric interview, and chart review data. We also evaluated the risk of CAD in these patients using the Framingham point system. There was no significant age difference in the MS prevalence rate in these patients. The young patients with schizophrenia in our study tended to have a higher prevalence of MS than the general population. In addition, female patients had a higher prevalence rate of MS than males. Based on the Framingham point system, we found the 10-year risk of CAD to be higher among the patients with schizophrenia than in the general population. Our study highlights the importance of the high risk of MS in both younger and older patients with schizophrenia, without a significant relationship to the use of antipsychotics. More complete cohort studies are needed to confirm these findings. Psychiatrists may want to establish more specific and detailed clinical guidelines for patients with chronic schizophrenia with comorbid physical diseases, especially MS and CAD. |
| SCZ Keywords | schizophrenia |
| 7 | Schizophr. Res. 2015 Dec 169: 186-92 |
| PMID | 26526751 |
| Title | Twelve-month psychosis-predictive value of the ultra-high risk criteria in children and adolescents. |
| Abstract | The validity of current ultra-high risk (UHR) criteria is under-examined in help-seeking minors, particularly, in children below the age of 12 years. Thus, the present study investigated predictors of one-year outcome in children and adolescents (CAD) with UHR status. Thirty-five children and adolescents (age 9-17 years) meeting UHR criteria according to the Structured Interview for Psychosis-Risk Syndromes were followed-up for 12 months. Regression analyses were employed to detect baseline predictors of conversion to psychosis and of outcome of non-converters (remission and persistence of UHR versus conversion). At one-year follow-up, 20% of patients had developed schizophrenia, 25.7% had remitted from their UHR status that, consequently, had persisted in 54.3%. No patient had fully remitted from mental disorders, even if UHR status was not maintained. Conversion was best predicted by any transient psychotic symptom and a disorganized communication score. No prediction model for outcome beyond conversion was identified. Our findings provide the first evidence for the predictive utility of UHR criteria in CAD in terms of brief intermittent psychotic symptoms (BIPS) when accompanied by signs of cognitive impairment, i.e. disorganized communication. However, because attenuated psychotic symptoms (APS) related to thought content and perception were indicative of non-conversion at 1-year follow-up, their use in early detection of psychosis in CAD needs further study. Overall, the need for more in-depth studies into developmental peculiarities in the early detection and treatment of psychoses with an onset of illness in childhood and early adolescence was further highlighted. |
| SCZ Keywords | schizophrenia |
| 8 | JAMA Psychiatry 2016 May 73: 472-80 |
| PMID | 27028160 |
| Title | Genome-wide Association Study of Cannabis Dependence Severity, Novel Risk Variants, and Shared Genetic Risks. |
| Abstract | Cannabis dependence (CAD) is a serious problem worldwide and is of growing importance in the United States because cannabis is increasingly available legally. Although genetic factors contribute substantially to CAD risk, at present no well-established specific genetic risk factors for CAD have been elucidated. To report findings for DSM-IV CAD criteria from association analyses performed in large cohorts of African American and European American participants from 3 studies of substance use disorder genetics. This genome-wide association study for DSM-IV CAD criterion count was performed in 3 independent substance dependence cohorts (the Yale-Penn Study, Study of Addiction: Genetics and Environment [SAGE], and International Consortium on the Genetics of Heroin Dependence [ICGHD]). A referral sample and volunteers recruited in the community and from substance abuse treatment centers included 6000 African American and 8754 European American participants, including some from small families. Participants from the Yale-Penn Study were recruited from 2000 to 2013. Data were collected for the SAGE trial from 1990 to 2007 and for the ICGHD from 2004 to 2009. Data were analyzed from January 2, 2013, to November 9, 2015. Criterion count for DSM-IV CAD. Among the 14 754 participants, 7879 were male, 6875 were female, and the mean (SD) age was 39.2 (10.2) years. Three independent regions with genome-wide significant single-nucleotide polymorphism associations were identified, considering the largest possible sample. These included rs143244591 (??=?0.54, P?=?4.32?×?10-10 for the meta-analysis) in novel antisense transcript RP11-206M11.7;rs146091982 (??=?0.54, P?=?1.33?×?10-9 for the meta-analysis) in the solute carrier family 35 member G1 gene (SLC35G1); and rs77378271 (??=?0.29, P?=?2.13?×?10-8 for the meta-analysis) in the CUB and Sushi multiple domains 1 gene (CSMD1). Also noted was evidence of genome-level pleiotropy between CAD and major depressive disorder and for an association with single-nucleotide polymorphisms in genes associated with schizophrenia risk. Several of the genes identified have functions related to neuronal calcium homeostasis or central nervous system development. These results are the first, to our knowledge, to identify specific CAD risk alleles and potential genetic factors contributing to the comorbidity of CAD with major depression and schizophrenia. |
| SCZ Keywords | schizophrenia |
| 9 | Psychopharmacology (Berl.) 2016 Jan 233: 19-37 |
| PMID | 26566609 |
| Title | The early identification of psychosis: can lessons be learnt from cardiac stress testing? |
| Abstract | Psychotic disorders including schizophrenia are amongst the most debilitating psychiatric disorders. There is an urgent need to develop methods to identify individuals at risk with greater precision and as early as possible. At present, a prerequisite for a diagnosis of schizophrenia is the occurrence of a psychotic episode. Therefore, attempting to detect schizophrenia on the basis of psychosis is analogous to diagnosing coronary artery disease (CAD) after the occurrence of a myocardial infarction (MI). The introduction of cardiac stress testing (CST) has revolutionized the detection of CAD and the prevention and management of angina and MI. In this paper, we attempt to apply lessons learnt from CST to the early detection of psychosis by proposing the development of an analogous psychosis stress test. We discuss in detail the various parameters of a proposed psychosis stress test including the choice of a suitable psychological or psychopharmacological "stressor," target population, outcome measures, safety of the approach, and the necessary evolution of test to become clinically informative. The history of evolution of CST may guide the development of a similar approach for the detection and management of psychotic disorders. The initial development of a test to unmask latent risk for schizophrenia will require the selection of a suitable and safe stimulus and the development of outcome measures as a prelude to testing in populations with a range of risk to determine predictive value. The use of CST in CAD offers the intriguing possibility that a similar approach may be applied to the detection and management of schizophrenia. |
| SCZ Keywords | schizophrenia |