PMC:2944667 / 30100-31571 JSONTXT

{"project":"TEST0","denotations":[{"id":"20877431-106-114-637216","span":{"begin":106,"end":110},"obj":"[\"19130314\"]"},{"id":"20877431-122-130-637217","span":{"begin":235,"end":239},"obj":"[\"9076854\"]"},{"id":"20877431-140-148-637218","span":{"begin":253,"end":257},"obj":"[\"10530632\"]"},{"id":"20877431-232-240-637219","span":{"begin":393,"end":397},"obj":"[\"11343862\"]"},{"id":"20877431-231-239-637220","span":{"begin":714,"end":718},"obj":"[\"17671870\"]"},{"id":"20877431-125-133-637221","span":{"begin":846,"end":850},"obj":"[\"9511926\"]"},{"id":"20877431-205-213-637222","span":{"begin":926,"end":930},"obj":"[\"11074872\"]"},{"id":"20877431-226-234-637223","span":{"begin":947,"end":951},"obj":"[\"11711858\"]"},{"id":"20877431-230-238-637224","span":{"begin":971,"end":975},"obj":"[\"18281411\"]"},{"id":"20877431-194-202-637225","span":{"begin":1172,"end":1176},"obj":"[\"9646890\"]"},{"id":"20877431-200-208-637226","span":{"begin":1178,"end":1182},"obj":"[\"17553960\"]"},{"id":"20877431-228-236-637227","span":{"begin":1206,"end":1210},"obj":"[\"9661250\"]"},{"id":"20877431-228-236-637228","span":{"begin":1227,"end":1231},"obj":"[\"15581715\"]"}],"text":"Altered hippocampal development has also been implicated in the pathogenesis of schizophrenia (Kobayashi, 2009). Total brain gray matter and hippocampal volumes are reduced at the time of first episode in schizophrenia (Ohnuma et al., 1997; Gur et al., 1999) and at times later in the disease course, volume reductions have been observed in PFC, hippocampus and temporal lobe (Shenton et al., 2001). Longitudinal studies with structural imaging show that both the PFC and the medial temporal lobe become progressively smaller during the period when psychosis develops and that dorsal prefrontal regions experience even more loss as illness progresses, consistent with a neurodegenerative process (Pantelis et al., 2007). Post mortem studies of the cerebral cortex of patients with schizophrenia have shown reductions in neuropil (Selemon et al., 1998), as well as in GABAergic cells expressing PV and reelin (Guidotti et al., 2000; Fatemi et al., 2001; Hashimoto et al., 2008). Post mortem analysis of the hippocampus also shows evidence for an abnormal GABAergic system and suggests that important signaling pathways are altered, including WNT and TGFbeta (Benes et al., 1998, 2007; Todtenkopf and Benes, 1998; Arnold et al., 2005). While these post mortem findings may reflect changes in the adult brain due to disease progression and medication effects, alterations in cortical neurodevelopmental processes could also create vulnerabilities that develop later in life."}

{"project":"0_colil","denotations":[{"id":"20877431-19130314-637216","span":{"begin":106,"end":110},"obj":"19130314"},{"id":"20877431-9076854-637217","span":{"begin":235,"end":239},"obj":"9076854"},{"id":"20877431-10530632-637218","span":{"begin":253,"end":257},"obj":"10530632"},{"id":"20877431-11343862-637219","span":{"begin":393,"end":397},"obj":"11343862"},{"id":"20877431-17671870-637220","span":{"begin":714,"end":718},"obj":"17671870"},{"id":"20877431-9511926-637221","span":{"begin":846,"end":850},"obj":"9511926"},{"id":"20877431-11074872-637222","span":{"begin":926,"end":930},"obj":"11074872"},{"id":"20877431-11711858-637223","span":{"begin":947,"end":951},"obj":"11711858"},{"id":"20877431-18281411-637224","span":{"begin":971,"end":975},"obj":"18281411"},{"id":"20877431-9646890-637225","span":{"begin":1172,"end":1176},"obj":"9646890"},{"id":"20877431-17553960-637226","span":{"begin":1178,"end":1182},"obj":"17553960"},{"id":"20877431-9661250-637227","span":{"begin":1206,"end":1210},"obj":"9661250"},{"id":"20877431-15581715-637228","span":{"begin":1227,"end":1231},"obj":"15581715"}],"text":"Altered hippocampal development has also been implicated in the pathogenesis of schizophrenia (Kobayashi, 2009). Total brain gray matter and hippocampal volumes are reduced at the time of first episode in schizophrenia (Ohnuma et al., 1997; Gur et al., 1999) and at times later in the disease course, volume reductions have been observed in PFC, hippocampus and temporal lobe (Shenton et al., 2001). Longitudinal studies with structural imaging show that both the PFC and the medial temporal lobe become progressively smaller during the period when psychosis develops and that dorsal prefrontal regions experience even more loss as illness progresses, consistent with a neurodegenerative process (Pantelis et al., 2007). Post mortem studies of the cerebral cortex of patients with schizophrenia have shown reductions in neuropil (Selemon et al., 1998), as well as in GABAergic cells expressing PV and reelin (Guidotti et al., 2000; Fatemi et al., 2001; Hashimoto et al., 2008). Post mortem analysis of the hippocampus also shows evidence for an abnormal GABAergic system and suggests that important signaling pathways are altered, including WNT and TGFbeta (Benes et al., 1998, 2007; Todtenkopf and Benes, 1998; Arnold et al., 2005). While these post mortem findings may reflect changes in the adult brain due to disease progression and medication effects, alterations in cortical neurodevelopmental processes could also create vulnerabilities that develop later in life."}

{"project":"2_test","denotations":[{"id":"20877431-19130314-38520493","span":{"begin":106,"end":110},"obj":"19130314"},{"id":"20877431-9076854-38520494","span":{"begin":235,"end":239},"obj":"9076854"},{"id":"20877431-10530632-38520495","span":{"begin":253,"end":257},"obj":"10530632"},{"id":"20877431-11343862-38520496","span":{"begin":393,"end":397},"obj":"11343862"},{"id":"20877431-17671870-38520497","span":{"begin":714,"end":718},"obj":"17671870"},{"id":"20877431-9511926-38520498","span":{"begin":846,"end":850},"obj":"9511926"},{"id":"20877431-11074872-38520499","span":{"begin":926,"end":930},"obj":"11074872"},{"id":"20877431-11711858-38520500","span":{"begin":947,"end":951},"obj":"11711858"},{"id":"20877431-18281411-38520501","span":{"begin":971,"end":975},"obj":"18281411"},{"id":"20877431-9646890-38520502","span":{"begin":1172,"end":1176},"obj":"9646890"},{"id":"20877431-17553960-38520503","span":{"begin":1178,"end":1182},"obj":"17553960"},{"id":"20877431-9661250-38520504","span":{"begin":1206,"end":1210},"obj":"9661250"},{"id":"20877431-15581715-38520505","span":{"begin":1227,"end":1231},"obj":"15581715"}],"text":"Altered hippocampal development has also been implicated in the pathogenesis of schizophrenia (Kobayashi, 2009). Total brain gray matter and hippocampal volumes are reduced at the time of first episode in schizophrenia (Ohnuma et al., 1997; Gur et al., 1999) and at times later in the disease course, volume reductions have been observed in PFC, hippocampus and temporal lobe (Shenton et al., 2001). Longitudinal studies with structural imaging show that both the PFC and the medial temporal lobe become progressively smaller during the period when psychosis develops and that dorsal prefrontal regions experience even more loss as illness progresses, consistent with a neurodegenerative process (Pantelis et al., 2007). Post mortem studies of the cerebral cortex of patients with schizophrenia have shown reductions in neuropil (Selemon et al., 1998), as well as in GABAergic cells expressing PV and reelin (Guidotti et al., 2000; Fatemi et al., 2001; Hashimoto et al., 2008). Post mortem analysis of the hippocampus also shows evidence for an abnormal GABAergic system and suggests that important signaling pathways are altered, including WNT and TGFbeta (Benes et al., 1998, 2007; Todtenkopf and Benes, 1998; Arnold et al., 2005). While these post mortem findings may reflect changes in the adult brain due to disease progression and medication effects, alterations in cortical neurodevelopmental processes could also create vulnerabilities that develop later in life."}