1.Pathogenic significance and possible pathogenic mechanism of human endogenous viruses in development of schizophrenia.
Chinese Journal of Virology 2014;30(1):98-102
The association between psychogenic illness and human endogenous viruses (HEVs), including human endogenous retrovirus and Borna disease virus, remains unclear. As the component of human genome, HEVs may become the joint of various pathogenic factors of schizophrenia (SZ), such as heredity, environment, and immunity. In this review, we strive to uncover the clinical and laboratory evidence for the roles and possible pathogenic mechanism of HEVs in the development of SZ.
Animals
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Environment
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Humans
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Schizophrenia
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etiology
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genetics
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immunology
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virology
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Viruses
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genetics
2.Measuring memory-prediction errors and their consequences in youth at risk for schizophrenia.
Richard S E KEEFE ; Michael S KRAUS
Annals of the Academy of Medicine, Singapore 2009;38(5):414-416
The largely consistent columnar circuitry observed throughout the cortex may serve to continuously predict bottom-up activation based on invariant memories. This "memory-prediction" function is essential to efficient and accurate perception. Many of the defined cognitive deficits associated with schizophrenia suggest a breakdown of memory-prediction function. As deficits in memory-prediction function are proposed to lie more proximal to the biological causes of schizophrenia than deficits in standard cognitive constructs, tests that more directly probe memory-prediction function may be especially sensitive predictors of conversion in individuals at high-risk for schizophrenia. In this article, we review the conceptual basis for this hypothesis, and outline how it may be tested with specific cognitive paradigms. The accurate identification of cognitive processes that precede the onset of psychosis will not only be useful for clinicians to predict which young people are at greatest risk for schizophrenia, but will also help determine the neurobiology of psychosis onset, thus leading to new and effective treatments for preventing schizophrenia and other psychoses.
Cognition Disorders
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Humans
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Memory
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Neuropsychological Tests
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Predictive Value of Tests
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Risk Assessment
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Schizophrenia
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etiology
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physiopathology
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Schizophrenic Psychology
4.Application Prospect of Integrative Omics in Forensic Identification of Methamphetamine-Associated Psychosis.
Long-Rui ZHAO ; Jian-Bo ZHANG ; Wei HAN ; Li ZHU ; Teng CHEN ; Fang-Lin GUAN
Journal of Forensic Medicine 2022;38(5):650-656
The clinical symptoms and signs of methamphetamine-associated psychosis (MAP) and schizophrenia are highly similar, but the situation is completely different when MAP and schizophrenia patients need to be assessed for criminal responsibility after they comitted a harmful behavior. Therefore, the distinction between the two psychoses is very important in forensic psychiatry. At present, the identification of these two psychoses is mainly dependent on the corresponding criteria such as the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and the Chinese Classification of Mental Disorders Version 3 (CCMD-3). It's challenging to diagnose and distinguish between the two in practical cases due to their similar clinical symptoms and the lack of effective objective indexes. Different from the limitations of single omics, integrative omics intergrates data from multiple dimensions and has been extensively studied in the field of schizophrenia and has achieved some preliminary results. In view of the correlation between MAP and schizophrenia and the potential application value of integrative omics, this paper proposes an integrative omics strategy for MAP pathogenesis and forensic identification, aiming to improve the further understanding of the relationship between the two psychoses and the corresponding pathogenesis. It also provides references for the future exploration of integrative omics in forensic precise identification and effective monitoring and early warning methods.
Humans
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Methamphetamine/adverse effects*
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Psychoses, Substance-Induced/etiology*
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Psychotic Disorders/genetics*
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Schizophrenia/genetics*
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Diagnosis, Differential
6.Cognitive dysfunction in schizophrenia: a perspective from the clinic to genetic brain mechanisms.
Annals of the Academy of Medicine, Singapore 2009;38(5):420-425
Schizophrenia is a brain disease with differing symptomatic presentations, outcomes, and complex genetic mechanisms. A selection of recent work integrating clinical observations, human brain imaging and genetics will be reviewed. While the mechanics of brain dysfunction in schizophrenia remains to be well understood, the emerging evidence suggests that a number of interacting genetic mechanisms in dopaminergic and glutamatergic systems affect fundamental disease-related cognitive brain processes and may do so early in disease neurodevelopment. The availability of new imaging and genetic technologies, and institutional support for research in the translational neurosciences, extends the hope that increased understanding of these brain processes could yield meaningful clinical applications.
Cognition Disorders
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etiology
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genetics
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Dopamine
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genetics
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Glutamic Acid
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genetics
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Humans
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Magnetic Resonance Imaging
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Neurosciences
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Schizophrenia
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genetics
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physiopathology
7.Imbalanced free radicals and antioxidant defense systems in schizophrenia: a comparative study.
Hui-chun LI ; Qiao-zhen CHEN ; Ying MA ; Jun-fu ZHOU
Journal of Zhejiang University. Science. B 2006;7(12):981-986
OBJECTIVETo examine changes of blood oxidative-antiovidative level in schizophrenic patients and its relationship with clinical symptoms.
METHODSForty-six Chinese patients met DSM-IV (Diagnostic and Statistical Manual of Mental Disorders-IV) criteria for schizophrenia and fifty age- and sex-matched healthy controls were enrolled in the present study. Baseline psychiatric symptom severity was assessed with brief psychiatric rating scale, positive and negative syndrome scale on the blood draw day. Fresh blood samples were collected to measure levels of nitric oxide and lipid peroxide in plasma as well as activities of superoxide dismutase, catalase and glutathione peroxidase in red blood cells by spectrophotometric assays simultaneously.
RESULTSComparison of the biochemical parameters indicated that the level of nitric oxide and lipid peroxide increased in patient group, which represented a positive correlation with positive scale scores; while the activities of three critical enzymes decreased and showed a negative linear correlation.
CONCLUSIONThis study showed that there are dysregulation of free radical metabolism and poor activities of the antioxidant defense systems in schizophrenic patients. Excess free radicals formation may play a critical role in the etiology of schizophrenia. Using antioxidants might be an effective therapeutic approach to partially alleviate or prevent the symptoms of schizophrenia.
Adolescent ; Adult ; Antioxidants ; metabolism ; Female ; Free Radicals ; Humans ; Lipid Peroxides ; metabolism ; Male ; Middle Aged ; Nitric Oxide ; metabolism ; Schizophrenia ; etiology ; metabolism
8.Research advances in add-on treatment for negative symptoms and cognitive dysfunction in schizophrenia.
Ranran LI ; Gangrui HEI ; Ye YANG ; Renrong WU ; Jingping ZHAO
Journal of Central South University(Medical Sciences) 2020;45(12):1457-1463
Antipsychotic medication is the primary treatment for schizophrenia, which is effective on ameliorating positive symptoms and can reduce the risk of recurrence, but it has limited efficacy for negative symptoms and cognitive dysfunction. The negative symptoms and cognitive dysfunction seriously affects the life quality and social function for the patients with schizophrenia. Currently, there is plenty evidence that antipsychotic drugs combined with adjuvant therapy drugs can effectively improve the negative symptoms and cognitive dysfunction. These drugs include anti-oxidants, nicotinic acetylcholine receptors and neuro-inflammatory drugs (anti-inflammatory drugs, minocycline), which show potential clinical effects.
Anti-Inflammatory Agents/therapeutic use*
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Antipsychotic Agents/therapeutic use*
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Cognitive Dysfunction/etiology*
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Humans
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Minocycline/therapeutic use*
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Schizophrenia/drug therapy*
9.Prevalence of metabolic syndrome among patients with schizophrenia in Singapore.
Jimmy LEE ; Milawaty NURJONO ; Audrey WONG ; Agus SALIM
Annals of the Academy of Medicine, Singapore 2012;41(10):457-462
INTRODUCTIONSchizophrenia has been associated with an increased risk of cardiometabolic morbidity and mortality. Metabolic syndrome (MetS), a reliable predictor of cardiovascular-related morbidity and mortality, has also been shown to be more prevalent in patients with schizophrenia. In this study, we investigated the prevalence of MetS in a sample of patients with schizophrenia in Singapore, and the potential risk factors associated with it.
MATERIALS & METHODSOne hundred patients with schizophrenia and 300 community controls were recruited. All subjects provided a fasted sample of venous blood to measure high-density lipoprotein cholesterol (HDL-C), triglycerides and glucose levels. Weight, height and waist circumference were measured. Presence of MetS was assessed according to the American Heart Association and the National Heart, Lung and Blood Institute (AHA/NHLBI) guidelines.
RESULTSThe prevalence of MetS in patients with schizophrenia was 46.0%. The adjusted odds ratio (OR) for MetS among patients was 2.79 (CI, 1.50 to 5.20, P = 0.001) when compared with controls. Increasing body mass index (BMI) was identifi ed to be signifi cantly associated with the prevalence of MetS.
CONCLUSIONThis study found a high prevalence of MetS in Singapore patients with schizophrenia, and that BMI might be a risk factor in the development of MetS. This information is clinically relevant as BMI is routinely measured in psychiatric practice today, and could be used to monitor for development of MetS in schizophrenia.
Adult ; Body Mass Index ; Case-Control Studies ; Female ; Humans ; Logistic Models ; Male ; Metabolic Syndrome ; diagnosis ; epidemiology ; etiology ; Odds Ratio ; Prevalence ; Risk Factors ; Schizophrenia ; complications ; Singapore ; Smoking ; adverse effects
10.Changes in expression levels of PV, GAD67 and KCC2 in the brain tissue of rats with schizophrenia induced by MK-801.
Yong LIU ; Ya-Mei TANG ; Xiang-Hui ZHANG ; Jing-Ping ZHAO
Chinese Journal of Contemporary Pediatrics 2012;14(11):869-874
OBJECTIVETo study changes in the expression levels of parvalbumin (PV), glutamate decarboxylase 67 (GAD67) and K+-Cl- cotransporter 2 (KCC2) in the brain tissue of rats with schizophrenia (SZ) induced by dizocilpine (MK-801), and to investigate the mechanism involving gamma-aminobutyric acid (GABA) by which NMDA receptor blocker induces SZ in the perinatal period.
METHODSThirty-six neonatal male Sprague-Dawley rats were randomly assigned to two batches on postnatal day 6. Each batch was divided into normal control (treated by 0.9% normal saline), SZ-development model (treated by subcutaneous injection of 0.1 mg/kg MK-801 on postnatal days 7-10; bid), and SZ-chronic medication model groups (treated by intraperitoneal injection of 0.2 mg/kg MK-801 on postnatal days 47-60; qd). On postnatal day 63, the brain tissue of the first batch of rats was obtained and then fixed with paraform for histological sections; expression levels of PV and GAD67 in the medial prefrontal cortex (mPFC) and hippocampus CA1 were measured by immunohistochemistry. Simultaneously, the second batch of rats was sacrificed and the mPFC and hippocampus were obtained and homogenized; expression levels of KCC2 in the mPFC and hippocampus were measured by Western blot.
RESULTSExpression levels of PV and GAD67 in the mPFC and hippocampus CA1 were significantly lower in the SZ-development and chronic medication model groups than in the normal control group (P<0.05). Expression levels of KCC2 in the mPFC and hippocampus were significantly lower in the SZ-development model group than in the SZ-chronic medication model and normal control groups (P<0.05).
CONCLUSIONSThe expression changes of PV and GAD67 in SZ can be simulated using the SZ development model induced by MK-801, which might affect the development of the GABA system in the PFC and hippocampus by downregulating KCC2 expression.
Animals ; CA1 Region, Hippocampal ; chemistry ; Dizocilpine Maleate ; pharmacology ; Glutamate Decarboxylase ; analysis ; Immunohistochemistry ; Male ; Parvalbumins ; analysis ; Prefrontal Cortex ; chemistry ; Rats ; Rats, Sprague-Dawley ; Schizophrenia ; etiology ; metabolism ; Symporters ; analysis