Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A large subgroup of around 25% of schizophrenia patients suffers from obsessive-compulsive symptoms (OCS) and about 12% fulfill the diagnostic criteria of an obsessive-compulsive disorder (OCD). The additional occurrence of OCS is associated with high subjective burden of disease, additional neurocognitive impairment, poorer social and vocational functioning, greater service utilization and high levels of anxiety and depression. Comorbid patients can be assigned to heterogeneous subgroups. One hypothesis assumes that second generation antipsychotics (SGAs), most importantly clozapine, might aggravate or even induce second-onset OCS. Several arguments support this assumption, most importantly the observed chronological order of first psychotic manifestation, start of treatment with clozapine and onset of OCS. In addition, correlations between OCS-severity and dose and serum levels and duration of clozapine treatment hint toward a dose-dependent side effect. It has been hypothesized that genetic risk-factors dispose patients with schizophrenia to develop OCS. One study in a South Korean sample reported associations with polymorphisms in the gene SLC1A1 (solute carrier family 1A1) and SGA-induced OCS. However, this finding could not be replicated in European patients. Preliminary results also suggest an involvement of polymorphisms in the BDNF gene (brain-derived neurotrophic factor) and an interaction between markers of SLC1A1 and the gene DLGAP3 (disc large associated protein 3) as well as GRIN2B (N-methyl-D-aspartate receptor subunit 2B). Further research of well-defined samples, in particular studies investigating possible interactions of genetic risk-constellations and pharmacodynamic properties, are needed to clarify the assumed development of SGA-induced OCS. Results might improve pathogenic concepts and facilitate the definition of at risk populations, early detection and monitoring of OCS as well as multimodal therapeutic interventions.
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PMID:Comorbid obsessive-compulsive symptoms in schizophrenia: contributions of pharmacological and genetic factors. 2395 Jul 45

This study tested the hypothesis that dietary L-arginine supplementation confers beneficial effects on growing pigs fed a mold-contaminated diet. The measured variables included: (1) the average daily weight gain and feed:gain ratio; (2) activities of total superoxide dismutase, glutathione peroxidase, diamine oxidase, as well as amino acid and D-lactate concentrations in serum; (3) intestinal morphology; (4) expression of the genes for SLC7A7 (amino acid transporter light chain, y(+L) system, family 7, member 7), SLC7A1 (cationic amino acid transporter, y(+) system, family 7, member 1), SLC1A1 (neuronal/epithelial high affinity glutamate transporter, system XAG, member 1), SLC5A1 (sodium/glucose cotransporter, family 5, member 1) in the ileum and jejunum. Mycotoxins in feedstuffs resulted in an enlarged small intestine mass, oxidative injury in tissues, and reduced growth performance in pigs. Dietary arginine supplementation enhanced (P < 0.05) expression of jejunal SLC7A7 and ileal SLC7A1, in comparison with the control and mycotoxin groups. In addition, supplementing 1% L-arginine to the mycotoxin-contaminated feed had the following beneficial effects (P < 0.05): (1) alleviating the imbalance of the antioxidant system in the body; (2) ameliorating intestinal abnormalities; and (3) attenuating whole-body growth depression, compared with the mycotoxin group without arginine treatment. Collectively, these results indicate that dietary supplementation with L-arginine exerts a protective role in pigs fed mold-contaminated foods. The findings may have important nutritional implications for humans and other mammals.
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PMID:Dietary arginine supplementation enhances intestinal expression of SLC7A7 and SLC7A1 and ameliorates growth depression in mycotoxin-challenged pigs. 2436 21

Insight into the biological pathomechanism of a clinical syndrome facilitates the development of effective interventions. This paper applies this perspective to the important clinical problem of obsessive-compulsive symptoms (OCS) occurring during the lifetime diagnosis of schizophrenia. Up to 25% of schizophrenia patients suffer from OCS and about 12% fulfil the diagnostic criteria of obsessive-compulsive disorder (OCD). This is accompanied by marked subjective burden of disease, high levels of anxiety, depression and suicidality, increased neurocognitive impairment, less favourable levels of social and vocational functioning, and greater service utilization. Comorbid patients can be assigned to heterogeneous subgroups. It is assumed that second generation antipsychotics (SGAs), most importantly clozapine, might aggravate or even induce second-onset OCS. Several epidemiological and pharmacological arguments support this assumption. Specific genetic risk factors seem to dispose patients with schizophrenia to develop OCS and risk-conferring polymorphisms has been defined in SLC1A1, BDNF, DLGAP3, and GRIN2B and in interactions between these individual genes. Further research is needed with detailed characterization of large samples. In particular interactions between genetic risk constellations, pharmacological and psychosocial factors should be analysed. Results will further define homogeneous subgroups, which are in need for differential causative interventions. In clinical practise, schizophrenia patients should be carefully monitored for OCS, starting with at-risk mental states of psychosis and longitudinal follow-ups, hopefully leading to the development of multimodal therapeutic interventions.
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PMID:Comorbid Obsessive-Compulsive Symptoms in Schizophrenia: Insight into Pathomechanisms Facilitates Treatment. 2655 9