Sentence examples for models for schizophrenia from inspiring English sources

Although the finding in rats was promising, developing animal models for schizophrenia and other brain diseases is extremely difficult, said Paul Greengard, professor of molecular and cellular neuroscience at Rockefeller University.

The validity of these animal preparations as animal models for schizophrenia is generally based upon the extent to which they induce measurable behavioral changes that are homologous or analogous to the core clinical features or the information processing endophenotypes (presymptom phenotypes) that are seen in schizophrenia.

Accordingly, several other cytokines such as IL-6, which are implicated in maternal immune models for schizophrenia, potentially involve EGF-NRG1 signaling as well.

Developing animal models for schizophrenia presents formidable challenges owing to the distinctively human nature of the symptoms that define it and the thus-far-obscured underlying biological mechanisms.

There is established evidence of NMDAR hypofunction [ 25] as a central component of the functional dysconnectivity; this is one of the most accepted models for schizophrenia [ 26].

Other studies have, at the same time, considered a number of psychological disorders without separately reporting the results of the regression model for schizophrenia patients [30 33].

Analyzing the results of the Maudsley Bethlem study, Gottesman and Shields devised the multi-element, polygenic causation model for schizophrenia.

For bipolar disorder, GSMA-Broad produconsistentlyntly stronger results than the GSMA-Best model; for schizophrenia, significance was split between GSMA-Broad (4 bins) and GSMA-Best (3 bins).

A similar hypothesis of disruption of hippocampal development has lead to a useful animal model of schizophrenia in which neonatal hippocampal lesions have good face and construct validity as a model for schizophrenia [61], [62].

Conversely, the present NRG1-Tg mice, which display the increases in these pathological markers, may be irrelevant to an animal model for schizophrenia in spite of their schizophrenia-like behavioral deficits.

If we assume the nuclear DNA model for schizophrenia, it should have many susceptibility genes of exceptionally high mutation rates; alternatively, it should have many disease-associated resistance genes of standard mutation rates on different chromosomes.