https://hal.archives-ouvertes.fr/hal-02437989/document

Opioid receptors: distinct roles in mood disorders

Schizophrenia has been conceived as a disorder of brain connectivity, but it is unclear how this network phenotype is related to the underlying genetics. We used morphometric similarity analysis of MRI data as a marker of interareal cortical connectivity in three prior case–control studies of psychosis: in total, n = 185 cases and n = 227 controls. Psychosis was associated with globally reduced morphometric similarity in all three studies. There was also a replicable pattern of case–control differences in regional morphometric similarity, which was significantly reduced in patients in frontal and temporal cortical areas but increased in parietal cortex. Using prior brain-wide gene expression data, we found that the cortical map of case–control differences in morphometric similarity was spatially correlated with cortical expression of a weighted combination of genes enriched for neurobiologically relevant ontology terms and pathways. In addition, genes that were normally overexpressed in cortical areas with reduced morphometric similarity were significantly up-regulated in three prior post mortem studies of schizophrenia. We propose that this combined analysis of neuroimaging and transcriptional data provides insight into how previously implicated genes and proteins as well as a number of unreported genes in their topological vicinity on the protein interaction network may drive structural brain network changes mediating the genetic risk of schizophrenia.

https://www.pnas.org/content/pnas/116/19/9604.full.pdf

Cortical patterning of abnormal morphometric similarity in psychosis is associated with brain expression of schizophrenia-related genes.

Schizophrenia is a severe mental disorder that affects approximately one percent of the general population. The pathogenesis of schizophrenia is influenced by many risk factors, both environmental and genetic. The environmental factors include the date of birth, place of birth and seasonal effects, infectious diseases, complications during pregnancy and delivery, substance abuse and stress. At the present time, in addition to environmental factors, genetic factors are assumed to play a role in the development of the schizophrenia. The heritability of schizo- phrenia is up to 80%. If one parent suffers from the condition, the probability that it will be passed down to the offspring is 13%. If it is present in both parents, the risk is more than 20%. The opinions are varied as to the risk factors affecting the development of schizophrenia. Knowing these factors may greatly contribute to prevention of the condition.

Epidemiology and risk factors of Schizophrenia

The µ-opioid receptor is a primary target for clinically important opioid analgesics, including morphine, fentanyl and methadone. Many genetic variations have been identified in the human µ-opioid receptor MOP gene (OPRM1), and their implications have been reported in the effects of opioid drugs and susceptibility to drug dependence. Interestingly, agonistic and antagonistic opioid effects are inversely associated with the A118G polymorphism genotype. The A118G polymorphism may also be associated with substance dependence and susceptibility to other disorders, including epilepsy and schizophrenia. The IVS1+A21573G, IVS1-T17286C, and TAA+A5359G polymorphisms in the OPRM1 gene may be associated with alcohol, opioid and tobacco dependence, respectively. However, some studies have failed to confirm the correlations between the polymorphisms and opioid effects and substance dependence. Further studies are needed to elucidate the molecular mechanisms underlying the effects of OPRM1 polymorphisms.

Pharmacogenomics of the human µ-opioid receptor

Endogenous opiates and behavior: 2010.

Schizophrenia is ranked among multifactor diseases in whose pathogenesis, besides environmental factors, an interplay of functional polymorphisms of a larger number of candidate genes is involved. Neurodevelopmental abnormities are among the most accepted hypotheses in the etiology of schizophrenia. Recently, the role of oligodendrocytes in the development of the cortex has been cited repeatedly. During their various phases of differentiation oligodendrocytes present on their surfaces diverse receptors, among others the μ-opioid receptor (OPRM1). The study was focused on the relationship between the functional A118G polymorphism of the OPRM1 gene (rs1799971) and schizophrenia in groups of 130 male patients and 452 male controls. An association study revealed yet unpublished statistically significant difference of allelic and genotypic frequencies between the control and patient groups. According to our present knowledge, we assume that the OPRM1 gene polymorphism can influence the myelination of CNS neurons through regulations of expression of OPRM1 receptors on surfaces of oligodendrocytes. The neuronal myelination seems to be one of the important factors in the pathogenesis of schizophrenia.

A118G Polymorphism of OPRM1 Gene is Associated with Schizophrenia

Přiciny schizofrenie jsou dnes vseobecně spojovany s poruchami
ve vývoji mozku. To mimo jine podporuji i prace poukazujici na
genetický zaklad abnormalniho neurovývoje u schizofrenie. V
nasi asociacni studii jsme se zabývali vztahem polymorfizmu
A118G genu pro OPRM1 ke schizofrenii. Z výsledků je patrný
statisticky významný rozdil alelických i genotypových frekvenci
mezi kontrolni skupinou a schizofreniky. Dle soucasných
poznatků se nabizi přicinna souvislost mezi polymorfizmem genu
pro OPRM1 a myelinizaci neuronů CNS, a to prostřednictvim
regulace exprese OPRM1 receptorů na povrchu oligodendrocytů.
Proces myelinizace se zda být významným faktorem patogeneze
schizofrenie.

Polymorfizmus genu pro OPRM1 a schizofrenie: nové výsledkyasociační studie

Impulsive and hyperactive behavior is related to a central serotonin dysfunction and the results of recent studies indicate the possible relationship between polymorphisms of the serotonin transporter gene and hyperkinetic disorder/ADHD. The sample included 90 boys with ADHD and the control group consisted of 82 boys. The diagnosis was based on the ICD-10 criteria and the Conners’ Parent Rating Scales. Attention was evaluated using the Shape Discrimination Test; TE-NA-ZO (Familiar Figures Finding Test) was used for impulsivity measures and a computerized set of Neurobehavioral Evaluation System (NES-2) was used for evaluation of both. The detection of the VNTR length polymorphism of the 5-HTT gene was done using the fragment analysis. The GeneMapper software was used for results analysis. Thirty-eight boys fulfilled the criteria of the Disturbance of activity and attention subtype (ICD-10; F90.0) and 52 of the Hyperkinetic conduct disorder (ICD-10; F90.1). The short S-allele and the SS-genotype was significantly more frequently (P<0.01) found in boys with hyperkinetic disorder compared to the control group. The results show a relationship between hyperkinetic disorder and the short all eles in contrast to studies published so far. It may be hypothesized that dysregulation in the 5-HT system could mainly influence the development of emotional and behavioral regulation in children with hyperkinetic disorder and reflects the symptomatology of hyperkinetic disorders as defined in ICD-10 rather than the narrower spectrum of symptoms of ADHD defined in DSM-IV.

/pdf/the-vntr-polymorphism-of-the-serotonin-transporter-gene-5a6gmu0vef.pdf

The VNTR Polymorphism of the Serotonin Transporter Gene Predisposes Czech Boys to Hyperkinetic Disorders

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A118G Polymorphism of OPRM1 Gene is Associated with Schizophrenia

Polymorfizmus genu pro OPRM1 a schizofrenie: nové výsledkyasociační studie

The VNTR Polymorphism of the Serotonin Transporter Gene Predisposes Czech Boys to Hyperkinetic Disorders