No association between schizophrenia and rs27388 of the MEGF10 gene in Chinese case–control sample

Yun, Libing; Gu, Yan; Hou, Yiping

doi:10.1016/j.psychres.2010.08.002

Cited by 3 publications

(3 citation statements)

References 5 publications

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“…Patients with schizophrenia exhibit a lower percentage passing even the compound discrimination, with large drops of those passing in those passing the extradimensional stage (Ceaser et al, 2008; Tyson et al, 2004). More recent data present error rates (Hilti et al, 2010; Yun et al, 2011). Evidence suggests that patients with schizophrenia, including medication-free first-episode patients, may have a generalized learning deficit that is not specific to extradimensional shifting (Hilti et al, 2010; Yun et al, 2011).…”

Section: Cross-species Cognitive Assessmentmentioning

confidence: 99%

“…More recent data present error rates (Hilti et al, 2010; Yun et al, 2011). Evidence suggests that patients with schizophrenia, including medication-free first-episode patients, may have a generalized learning deficit that is not specific to extradimensional shifting (Hilti et al, 2010; Yun et al, 2011). The primary outcome presented for the rodent ASST is that of trials to criterion for each stage, with more trials required at the extradimensional versus intradimensional stage.…”

Section: Cross-species Cognitive Assessmentmentioning

confidence: 99%

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Developing treatments for cognitive deficits in schizophrenia: The challenge of translation

2014

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Schizophrenia is a life-long debilitating mental disorder affecting tens of millions of people worldwide. The serendipitous discovery of antipsychotics focused pharmaceutical research on developing a better antipsychotic. Our understanding of the disorder has advanced however, with the knowledge that cognitive enhancers are required for patients in order to improve their everyday lives. Whilst antipsychotics treat psychosis, they do not enhance cognition and hence are not antischizophrenics. Developing pro-cognitive therapeutics has been extremely difficult however, especially when no approved treatment exists. In lieu of stumbling on an efficacious treatment, developing targeted compounds can be facilitated by understanding the neural mechanisms underlying altered cognitive functioning in patients. Equally importantly, these cognitive domains will need to be measured similarly in animals and humans so that novel targets can be tested prior to conducting expensive clinical trials. To date, the limited similarity of testing across species has resulted in a translational bottleneck. In this review, we emphasize that schizophrenia is a disorder characterized by abnormal cognitive behavior. Quantifying these abnormalities using tasks having cross-species validity would enable the quantification of comparable processes in rodents. This approach would increase the likelihood that the neural substrates underlying relevant behaviors will be conserved across species. Hence, we detail cross-species tasks which can be used to test the effects of manipulations relevant to schizophrenia and putative therapeutics. Such tasks offer the hope of providing a bridge between non-clinical and clinical testing that will eventually lead to treatments developed specifically for patients with deficient cognition.

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Section: Cross-species Cognitive Assessmentmentioning

confidence: 99%

Section: Cross-species Cognitive Assessmentmentioning

confidence: 99%

Developing treatments for cognitive deficits in schizophrenia: The challenge of translation

2014

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“…Pathways affected include immune responses, neurology, amyloidosis and cognition, behavior, and seizure. Blood brain barrier, brain damage, edema, and headache pathway effects, as well as a potential schizophrenia nodes with connections to MEGF10 and MEGF11 which binds Atrophin 1 (ATN1) a seizure related protein also appear [6,[45][46][47][48][49]. Of note, some of the proteins listed in Table 3 Table 3 having a 2x ratio difference for both the number of hits and the number of sera observed were analyzed using bioinformatics software.…”

Section: Plos Onementioning

confidence: 99%

Distinguishing patients with idiopathic epilepsy from solitary cysticercus granuloma epilepsy and biochemical phenotype assessment using a serum biomolecule profiling platform

et al. 2020

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A major source of epilepsy is Neurocysticercosis (NCC), caused by Taenia solium infection. Solitary cysticercus granuloma (SCG), a subgroup of NCC induced epilepsy, is the most common form of NCC in India. Current diagnostic criteria for SCG epilepsy require brain imaging which may not be available in communities where the disease is endemic. Identification of serum changes and potential biomolecules that could distinguish SCG epilepsy from idiopathic generalized epilepsy (IE), without the initial need for imaging, could assist in disease identification, understanding, and treatment. The objective here was to investigate, using mass spectrometry (MS), sera biomolecule differences between patients with SCG epilepsy or IE to help distinguish these disorders based on physiological differences, to understand underlying phenotypes and mechanisms, and to lay ground work for future therapeutic and biomarker analyses. Sera were obtained from patients with SCG or IE (N = 29 each group). Serum mass peak profiling was performed with electrospray ionization (ESI) MS, and mass peak area means in the two groups were compared using leave one [serum sample] out cross validation (LOOCV). Serum LOOCV analysis identified significant differences between SCG and IE patient groups (p = 10 −20), which became non-significant (p = 0.074) when the samples were randomly allocated to the groups and reanalyzed. Tandem MS/MS peptide analysis of serum mass peaks from SCG or IE patients was performed to help identify potential peptide/protein biochemical and phenotypic changes involving these two forms of epilepsy. Bioinformatic analysis of these peptide/protein changes suggested neurological, inflammatory, seizure, blood brain barrier, cognition, ion channel, cell death, and behavior related biochemical systems were being altered in these disease states. This

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Significance of the Hardy–Weinberg equilibrium in genetic association studies

Saadat

2011

Psychiatry Research

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No association between schizophrenia and rs27388 of the MEGF10 gene in Chinese case–control sample

Cited by 3 publications

References 5 publications

Developing treatments for cognitive deficits in schizophrenia: The challenge of translation

Developing treatments for cognitive deficits in schizophrenia: The challenge of translation

Distinguishing patients with idiopathic epilepsy from solitary cysticercus granuloma epilepsy and biochemical phenotype assessment using a serum biomolecule profiling platform

Significance of the Hardy–Weinberg equilibrium in genetic association studies

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