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

According to the Diagnostic and Statistical Manual of Mental Disorders, 4 out of the 10 leading causes of disability in the US and other developed countries are mental disorders. Major depression, bipolar disorder, schizophrenia, and obsessive compulsive disorder (OCD) are among the most common mental disorders that currently plague numerous countries and have varying incidence rates from 26 percent in America to 4 percent in China. Though some of this difference may be attributable to the manner in which individual healthcare providers diagnose mental disorders, this noticeable distribution can be also explained by studies which show that a lack of certain dietary nutrients contribute to the development of mental disorders. Notably, essential vitamins, minerals, and omega-3 fatty acids are often deficient in the general population in America and other developed countries; and are exceptionally deficient in patients suffering from mental disorders. Studies have shown that daily supplements of vital nutrients often effectively reduce patients' symptoms. Supplements that contain amino acids also reduce symptoms, because they are converted to neurotransmitters that alleviate depression and other mental disorders. Based on emerging scientific evidence, this form of nutritional supplement treatment may be appropriate for controlling major depression, bipolar disorder, schizophrenia and anxiety disorders, eating disorders, attention deficit disorder/attention deficit hyperactivity disorder (ADD/ADHD), addiction, and autism. The aim of this manuscript is to emphasize which dietary supplements can aid the treatment of the four most common mental disorders currently affecting America and other developed countries: major depression, bipolar disorder, schizophrenia, and obsessive compulsive disorder (OCD). Most antidepressants and other prescription drugs cause severe side effects, which usually discourage patients from taking their medications. Such noncompliant patients who have mental disorders are at a higher risk for committing suicide or being institutionalized. One way for psychiatrists to overcome this noncompliance is to educate themselves about alternative or complementary nutritional treatments. Although in the cases of certain nutrients, further research needs to be done to determine the best recommended doses of most nutritional supplements, psychiatrists can recommend doses of dietary supplements based on previous and current efficacious studies and then adjust the doses based on the results obtained.
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PMID:Nutritional therapies for mental disorders. 1820 98

This paper describes a new bioinformatic tool for use in psychiatric research, "SLEP" (Sullivan Lab Evidence Project). SLEP is a searchable archive of findings from psychiatric genetics that is freely available on the web for non-commercial use (http://slep.unc.edu). Via a simple interface, users can retrieve findings from genome-wide linkage, genome-wide association, and microarray studies for ADHD, autism, bipolar disorder, eating disorders, major depression, nicotine dependence, and schizophrenia. Findings can be save to disk or viewed via a genome browser.
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PMID:A searchable database of genetic evidence for psychiatric disorders. 1854 8

The histamine H3 receptor is a pre-synaptic auto- and hetero-receptor that controls the release of histamine and a variety of other neurotransmitters in the brain. As such, modulation of the histamine H(3) receptor is expected to affect wake via control of the release of histamine and to affect cognition via regulation of several other neurotransmitters including acetylcholine and norepinephrine. Over the last several years numerous pre-clinical studies have shown that histamine H3 antagonists promote wakefulness, improve cognition, and in some cases affect food intake. Based on the interest level generated from these early pharmacology studies, and following the cloning and expression of the human histamine H3 receptor, many pharmaceutical companies began drug discovery programs aimed at the identification of histamine H3 antagonists suitable for human clinical trials. These efforts have led to many new chemotypes, and several promising compounds have recently entered the clinic for a variety of conditions, including ADHD, Narcolepsy, EDS associated with Narcolepsy, Cognitive disorders and Schizophrenia. Recent efforts towards the identification and pharmacological characterization of novel histamine H3 antagonists will be discussed.
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PMID:Histamine H3 antagonists as wake-promoting and pro-cognitive agents. 1867 68

Prepulse inhibition of startle (PPI) is a measure of sensorimotor gating, a pre-conscious regulator of attention. PPI is impaired in adults with schizophrenia and several other neuropsychiatric disorders associated with attentional abnormalities. The core feature of ADHD involves deficits in attention and, like schizophrenia, ADHD is associated with dysregulation of cortical-striatal circuits and dopamine transmission. Therefore, PPI may be disrupted in ADHD. While ADHD persists into adulthood in approximately half the children with ADHD, there has not been any published report of PPI in ADHD adults. In this study, PPI was measured in a sample of ADHD adults and compared to a sample of healthy comparison (HC) subjects. Twenty unmedicated adults with ADHD (11 inattentive subtype, 9 combined subtype) and 17 HC subjects were administered an eyeblink startle PPI paradigm. The PPI of ADHD adults was not significantly different from that of HC subjects in any of the PPI conditions. There was no significant effect of ADHD subtype nor of gender. The lack of PPI deficits in ADHD adults has important implications and suggests that, despite the presence of PPI dysregulation in a large number of disparate neuropsychiatric disorders, it is not a general feature of all neuropsychiatric disorders with attention abnormalities. Furthermore, the attentional deficiency in ADHD may have a neurobiological substrate somewhat distinct from schizophrenia and other neuropsychiatric disorders that are associated with PPI deficits. This distinction may be related to a relative sparing of pre-conscious attentional functions in ADHD compared to other disorders with PPI impairment.
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PMID:Prepulse inhibition of startle in adults with ADHD. 1867 83

Several neurodevelopmental disorders, including schizophrenia, autism, ADD/ADHD and dyslexia are believed to originate during gestation and involve white matter abnormalities. Modulation of glutamate environments and glutamate receptors has also been implicated in alteration of oligodendrocytes, the myelin forming cells of the CNS. To begin to understand how modulation of the glutamate system affects the maturation of oligodendrocytes, developing rats were subjected to prenatal blockade of the NMDA receptor with phencyclidine (PCP). Oligodendrocyte development and differentiation were then examined postnatally by measuring markers for early, middle and late stage cells. The results indicate that, while the level of marker proteins for neurons and astrocytes remains the same, early oligodendrocyte progenitor cell markers are decreased in rat brains prenatally exposed to PCP. Labeling of cells of intermediate, immature cell stages is elevated. Late stage markers for myelinating oligodendrocytes are subsequently decreased. These data suggest that prenatal NMDA receptor blockade reduces the level of progenitors and that the surviving cells are arrested at an immature stage. This premature arrest appears to result in fewer fully differentiated, mature oligodendrocytes that are capable of producing myelin. These results have interesting implications for the role of glutamate and glutamate receptors in white matter abnormalities in neurodevelopmental disorders.
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PMID:In utero PCP exposure alters oligodendrocyte differentiation and myelination in developing rat frontal cortex. 1867 60

Psychotropic drugs acting on monoamine neurotransmission are major pharmacological treatments for neuropsychiatric conditions such as schizophrenia, depression, bipolar disorder, Tourette syndrome, ADHD, and Alzheimer disease. Independent lines of research involving biochemical and behavioral approaches in normal and/or genetically modified mice provide converging evidence for an involvement of the signaling molecules Akt and glycogen synthase kinase-3 (GSK3) in the regulation of behavior by dopamine and serotonin (5-HT). These signaling molecules have also received attention for their role in the actions of psychoactive drugs such as antidepressants, antipsychotics, lithium, and other mood stabilizers. Furthermore, investigations of the mechanism by which D2 dopamine receptors regulate Akt/GSK3 signaling strongly support the physiological relevance of a new modality of G protein-coupled receptor (GPCR) signaling involving the multifunctional scaffolding protein beta-arrestin 2. Elucidation of the contribution of multiple signaling pathways to the action of psychotropic drugs may provide a better biological understanding of psychiatric disorders and lead to more efficient therapeutics.
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PMID:Akt/GSK3 signaling in the action of psychotropic drugs. 1892 2

Psychiatric comorbidity is defined as the co-occurrence of a psychiatric disorder in a patient with a substance use disorder. Psychiatric disorders in substance abuse patients can antedate the substance use disorder or be a consequence of the substance abuse. There is emerging evidence that drug use in adolescence may alter the onset of certain psychiatric disorders in vulnerable individuals. Patients with concurrent comorbid disorders present special challenges for the substance abuse treatment system in terms of diagnosis and management because each disorder has the capability of exacerbating the other. This manuscript is a summary of an ISAM symposium that featured three speakers who discussed the following topics: 1. Etiology and treatment of comorbid psychiatric and substance use disorders in adolescents; 2. Treatment of ADHD and substance use disorders in adults; 3. Effects of substance abuse on the onset, severity, and treatment of schizophrenia. Recommendations for further research will be presented.
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PMID:Comorbid psychiatric and substance abuse disorders: recent treatment research. 1904 6

Synaptosomal Associated Protein 25 kDa (SNAP25) has been implicated in the pathogenesis of schizophrenia by numerous neuropathological studies and genetic variation at SNAP25 has been reported to be associated with ADHD. Expression levels of the putative schizophrenia susceptibility gene DTNBP1 has been shown to influence the levels of SNAP25 in vitro. We undertook directed mutation screening of SNAP25 in UK schizophrenic cases followed by direct association analysis of all variants identified and identified known exonic SNPs that showed evidence for association (rs3746544 P = 0.004 OR = 1.26, rs8636 P = 0.003 OR = 1.27), although these SNPs are highly correlated (r(2) > 0.99). We additionally genotyped a further 31 tag SNPs spanning the SNAP25 locus and identified several independent SNPs that were nominally associated with schizophrenia (strongest association at rs3787283, P = 0.006, OR = 1.25) however, due to the number of tests performed no SNP met experiment-wise significance (minimum permuted P-value = 0.1). Post hoc analysis revealed that the SNPs nominally associated with schizophrenia (rs3787283, rs3746544) were the same as those previously demonstrated to be associated with ADHD but with the opposite alleles, allowing the intriguing hypothesis that genetic variation at SNAP25 may be differentially associated with both schizophrenia and ADHD.
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PMID:Evidence that putative ADHD low risk alleles at SNAP25 may increase the risk of schizophrenia. 1913 10

Deficient prepulse inhibition (PPI) of startle reflects disturbed sensorimotor gating found in certain neuropsychiatric disorders, such as Tourette's syndrome, ADHD, Huntington's and schizophrenia. We here tested, whether lesions of the entopeduncular nucleus (EPN) would improve a PPI-deficit induced by selective breeding. Rats with breeding induced high and low expression of PPI were stereotaxically microinjected with ibotenate (0.2 microg in 0.3 microl phosphate buffered saline) or vehicle into the EPN and two weeks later tested for PPI of the acoustic startle response (ASR) and motor activity. Lesions of the EPN counteracted the breeding-induced PPI-deficit and reduced ASR in the PPI low group without affecting their motor activity. In the PPI high group EPN lesions did not affect PPI, ASR, and motor activity. This work indicates an important role of the EPN in the modulation of sensorimotor gating. Additionally, PPI low rats may provide a non-pharmacological model that can be used to develop new therapeutic strategies for neuropsychiatric disorders.
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PMID:Deficient sensorimotor gating induced by selective breeding in rats is improved by entopeduncular nucleus lesions. 1923 72

Smoking is a leading cause of morbidity and premature mortality in the United States. The relationship between tobacco smoking and several forms of cancer, heart disease, stroke, chronic lung disease, and other medical diseases is well recognized and accepted. Recent epidemiological studies are now focusing on the link between tobacco use and psychiatric diseases. Experts now suggest that in the differential diagnosis of "smoker," depression, alcohol dependence, and schizophrenia are highest on the list. Studies are also focusing on the role of secondhand tobacco exposure, either in utero or during childhood, in the risk of dual disorders. Prenatal exposure may alter gene expression and change the risk for a variety of life-long psychiatric diseases, e.g., ADD/ADHD, antisocial personality disorders, substance use disorders, and major depression. Considerable time and effort have been devoted to studying the link between smoking and depression and also schizophrenia. We will focus on less well-studied areas in tobacco use and psychiatric dual disorders (including eating disorders), prenatal and early childhood secondhand smoke (SHS) exposure, and the relationship to the genesis of these dual disorders.
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PMID:Tobacco and psychiatric dual disorders. 1928 70


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