PMC:2944667 / 31572-32770 JSONTXT

{"project":"TEST0","denotations":[{"id":"20877431-159-167-637229","span":{"begin":417,"end":421},"obj":"[\"15240797\"]"},{"id":"20877431-116-124-637230","span":{"begin":540,"end":544},"obj":"[\"19379776\"]"},{"id":"20877431-138-146-637231","span":{"begin":562,"end":566},"obj":"[\"19828788\"]"},{"id":"20877431-162-170-637232","span":{"begin":586,"end":590},"obj":"[\"19502360\"]"},{"id":"20877431-230-238-637233","span":{"begin":947,"end":951},"obj":"[\"19805316\"]"}],"text":"Genes that are implicated in stem cell regulation, including neuregulin, disc-1, wnt related genes, bdnf and fgfr1, have been associated with schizophrenia in genetic association and post mortem studies, suggesting NSCs dysregulation in at least some cases. Mouse models lacking fgfr1 embryonically have smaller hippocampi and cortical interneuron deficits similar to those in patients with psychosis (Ohkubo et al., 2004). Similarly, deficient bdnf, neuregulin and disc-1 genes in mice mimic various aspects of the disorder (Ayhan et al., 2009; Brandon et al., 2009; Meyer and Morris, 2009). Conversely, mutations found in some patients with schizophrenia have significant effects on cortical stem cell development. Mice lacking the genes within the 22q11 mutation (velocardiofacial syndrome, a known chromosomal abnormality predisposing to schizophrenia) have abnormal neurogenesis, specifically affecting upper cortical layers (Meechan et al., 2009). As in autism, patients with schizophrenia are likely heterogenous, with pathology in some determined by a component of neuronal functioning that arises postnatally and in others, determined by earlier disruptions of patterning and neurogenesis."}

{"project":"0_colil","denotations":[{"id":"20877431-15240797-637229","span":{"begin":417,"end":421},"obj":"15240797"},{"id":"20877431-19379776-637230","span":{"begin":540,"end":544},"obj":"19379776"},{"id":"20877431-19828788-637231","span":{"begin":562,"end":566},"obj":"19828788"},{"id":"20877431-19502360-637232","span":{"begin":586,"end":590},"obj":"19502360"},{"id":"20877431-19805316-637233","span":{"begin":947,"end":951},"obj":"19805316"}],"text":"Genes that are implicated in stem cell regulation, including neuregulin, disc-1, wnt related genes, bdnf and fgfr1, have been associated with schizophrenia in genetic association and post mortem studies, suggesting NSCs dysregulation in at least some cases. Mouse models lacking fgfr1 embryonically have smaller hippocampi and cortical interneuron deficits similar to those in patients with psychosis (Ohkubo et al., 2004). Similarly, deficient bdnf, neuregulin and disc-1 genes in mice mimic various aspects of the disorder (Ayhan et al., 2009; Brandon et al., 2009; Meyer and Morris, 2009). Conversely, mutations found in some patients with schizophrenia have significant effects on cortical stem cell development. Mice lacking the genes within the 22q11 mutation (velocardiofacial syndrome, a known chromosomal abnormality predisposing to schizophrenia) have abnormal neurogenesis, specifically affecting upper cortical layers (Meechan et al., 2009). As in autism, patients with schizophrenia are likely heterogenous, with pathology in some determined by a component of neuronal functioning that arises postnatally and in others, determined by earlier disruptions of patterning and neurogenesis."}

{"project":"2_test","denotations":[{"id":"20877431-15240797-38520506","span":{"begin":417,"end":421},"obj":"15240797"},{"id":"20877431-19379776-38520507","span":{"begin":540,"end":544},"obj":"19379776"},{"id":"20877431-19828788-38520508","span":{"begin":562,"end":566},"obj":"19828788"},{"id":"20877431-19502360-38520509","span":{"begin":586,"end":590},"obj":"19502360"},{"id":"20877431-19805316-38520510","span":{"begin":947,"end":951},"obj":"19805316"}],"text":"Genes that are implicated in stem cell regulation, including neuregulin, disc-1, wnt related genes, bdnf and fgfr1, have been associated with schizophrenia in genetic association and post mortem studies, suggesting NSCs dysregulation in at least some cases. Mouse models lacking fgfr1 embryonically have smaller hippocampi and cortical interneuron deficits similar to those in patients with psychosis (Ohkubo et al., 2004). Similarly, deficient bdnf, neuregulin and disc-1 genes in mice mimic various aspects of the disorder (Ayhan et al., 2009; Brandon et al., 2009; Meyer and Morris, 2009). Conversely, mutations found in some patients with schizophrenia have significant effects on cortical stem cell development. Mice lacking the genes within the 22q11 mutation (velocardiofacial syndrome, a known chromosomal abnormality predisposing to schizophrenia) have abnormal neurogenesis, specifically affecting upper cortical layers (Meechan et al., 2009). As in autism, patients with schizophrenia are likely heterogenous, with pathology in some determined by a component of neuronal functioning that arises postnatally and in others, determined by earlier disruptions of patterning and neurogenesis."}