Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Schizophrenia and depression are two common and debilitating psychiatric conditions. Up to 61% of schizophrenic patients have comorbid clinical depression, often undiagnosed. Both share significant overlaps in underlying biological processes, which are relevant to the course and treatment of both conditions. Shared processes include changes in cell-mediated immune and inflammatory pathways, e.g. increased levels of pro-inflammatory cytokines and a Th1 response; activation of oxidative and nitrosative stress (O&NS) pathways, e.g. increased lipid peroxidation, damage to proteins and DNA; decreased antioxidant levels, e.g. lowered coenzyme Q10, vitamin E, glutathione and melatonin levels; autoimmune responses; and activation of the tryptophan catabolite (TRYCAT) pathway through induction of indoleamine-2,3-dioxygenase. Both show cognitive and neurostructural evidence of a neuroprogressive process. Here we review the interlinked nature of these biological processes, suggesting that schizophrenia is immunologically primed for an increased expression of depression. Such a conceptualization explains, and incorporates, many of the current perspectives on the nature of schizophrenia and depression, and has implications for the nature of classification and treatment of both disorders. An early developmental etiology to schizophrenia, driven by maternal infection, with subsequent impact on offspring immuno-inflammatory responses, creates alterations in the immune pathways, which although priming for depression, also differentiates the two disorders.
 ...
PMID:Schizophrenia is primed for an increased expression of depression through activation of immuno-inflammatory, oxidative and nitrosative stress, and tryptophan catabolite pathways. 2293 36

Objective: Mitochondrial dysfunction has been implicated in the pathophysiology of schizophrenia and other neuropsychiatric disorders. Though the exact mechanisms and clinical implications for this dysfunction are not fully determined, there is a hypothesis that deficiency in coenzyme Q10 (CoQ10) may contribute to mitochondrial impairments and be reflected in cognitive, affective, and energy disturbances in the disorders. CoQ10 is a critical component of the mitochondrial respiratory chain and an essential free radical scavenger, necessary for mitochondrial function. Here, we review the results of CoQ10 supplementation interventions for adults with various neurological and neuropsychiatric disorders and consider the therapeutic potential of CoQ10 supplementation for schizophrenia in light of these studies. Methods: A literature review of randomised controlled trials and open-label studies investigating the effect of CoQ10 as a single intervention in adults with neurological and neuropsychiatric disorders was conducted. Results: CoQ10 supplementation has some positive effects on fatigue, cognitive impairment and affective difficulties in several neurological and neuropsychiatric conditions with associated mitochondrial dysfunction. Discussion: CoQ10 may be of therapeutic value to schizophrenia given evidence of mitochondrial dysfunction in the disorder.
 ...
PMID:Coenzyme Q10 and neuropsychiatric and neurological disorders: relevance for schizophrenia. 3053 8

Thioridazine (TZ) is used mainly in the treatment of schizophrenia. However, hepatotoxicity as a life-threatening adverse effect is associated with its clinical use. In this context, we examined the cytotoxic mechanisms of TZ on freshly isolated rat hepatocytes to better understanding of the pathogenesis of TZ-induced hepatotoxicity. Hepatocytes were prepared by the method of collagenase enzyme perfusion via the portal vein. The level of parameters such as cell death, reactive oxygen species (ROS) formation, lipid peroxidation (LPO), mitochondrial membrane potential (MMP), lysosomal membrane integrity and cellular glutathione (GSH) content in TZ-treated and non-treated hepatocytes were determined and the mentioned markers were assessed in the presence of Coenzyme Q10 and/or melatonin. Results showed that TZ caused an increase in ROS formation as well as induction of LPO and GSH depletion. Moreover, mitochondria and lysosomes seem to be targets of TZ-induced toxicity. The administration of Coenzyme Q10 and/or melatonin efficiently decreased the rate of ROS formation, LPO and improved cell viability, MMP, GSH level and lysosome membrane integrity. This study proposes the possible protective role of Coenzyme Q10 and/or melatonin against TZ-induced cellular injury probably through their radical scavenging properties and their effects on mitochondria and lysosomes.
 ...
PMID:Mechanistic Approach for Thioridazine-Induced Hepatotoxicity and Potential Benefits of Melatonin and/or Coenzyme Q10 on Freshly Isolated Rat Hepatocytes. 3056 4

Comorbidities, dietary supplement use, and prescription drug use may negatively (or positively) affect mental health in cardiovascular patients. Although the significance of mental illnesses, such as depression, anxiety, and schizophrenia, on cardiovascular disease is well documented, mental illnesses resulting from heart disease are not well studied. In this paper, we introduce the risk factors of mental illnesses as an exploratory study and develop a prediction framework for mental illness that uses comorbidities, dietary supplements, and drug usage in heart disease patients. Particularly, the data used in this study consist of the records of 68,647 patients with heart disease, including the patient's mental illness information and the patient's intake of dietary supplements, antibiotics, and comorbidities. Patients in age groups <61, gender differences, and drug intakes, such as Azithromycin, Clarithromycin, Vitamin B6, and Coenzyme Q10, were associated with mental illness. For predictive modeling, we consider applying various state-of-the-art machine learning techniques with tuned parameters and finally obtain the following: Depression: 78.01% accuracy, 79.13% sensitivity, 72.65% specificity, and 86.26% Area Under the Curve (AUC). Anxiety: 82.93% accuracy, 82.86% sensitivity, 83.35% specificity, and 88.45% AUC. Schizophrenia: 87.59% accuracy, 87.70% sensitivity, 85.14% specificity, and 92.73% AUC. Disease: 86.63% accuracy, 95.50% sensitivity, 77.76% specificity, and 91.59% AUC. From the results, we conclude that using heart disease information, comorbidities, dietary supplement use, and antibiotics enables us to accurately predict the mental health outcome.
 ...
PMID:Prediction of Mental Illness in Heart Disease Patients: Association of Comorbidities, Dietary Supplements, and Antibiotics as Risk Factors. 3318 35