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10.1097/HRP.0000000000000102 http://scihub22266oqcxt.onion/10.1097/HRP.0000000000000102 C4788103!4788103!26954593     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Harv+Rev+Psychiatry 2016 ; 24 (2): 80-6 Nephropedia Template TP {{tp|p=26954593|t=2016. A Perspective on the history of the concept of ?disconnectivity? in schizophrenia |pdf=|usr=}}{{26954593}} gab.com Text A Perspective on the history of the concept of disconnectivity in schizophrenia JO: Harv Rev Psychiatry http://www.kidney.de/pget.php?&tw=1&pmid=26954593 #FOAvip Nearly sixty years ago Seymour Kety proposed that research on genetics and brain pathology but not on neurochemistry would ultimately lead to an understanding of the pathophysiology of schizophrenia. This Perspective will demonstrate how prescient Kety?s proposal was as advances in research on brain structure and on genetics have shaped our current understanding of the pathophysiology of schizophrenia. Brain imaging techniques have shown that schizophrenia is associated with cortical atrophy and ventricular enlargement, which progresses for at least a decade after the onset of psychosis. Cortical atrophy correlates with negative symptoms and cognitive impairment but not with psychosis in schizophrenia. Studies with the Golgi staining technique that illuminates the entire neuron indicate that cortical atrophy was due to reduced synaptic connectivity on the pyramidal neurons and not due to actual loss of neurons. Results of recent genetic studies indicate that several risk genes for schizophrenia are within two degrees of separation from the N-methy-D-aspartate (NMDA) receptor, a subtype of glutamate receptor that is critical to synapse formation and synaptic plasticity. Inactivation of one of these risk genes encoding serine racemase, which synthesizes D-serine, a co-agonist of the NMDA receptor, reproduces the synaptic pathology of schizophrenia. Thus, widespread loss of cortical synaptic connectivity appears to be the primary pathology in schizophrenia that is driven by multiple risk genes that adversely affect synaptogenesis and maintenance as hypothesized by Kety. Twit Text FOAVip A Perspective on the history of the concept of disconnectivity in schizophrenia ????Harv Rev Psychiatry http://www.kidney.de/pget.php?&tw=1&pmid=26954593 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26954593 #FOAvip English Wikipedia <ref>{{Cite pmid|26954593}}</ref> A Perspective on the history of the concept of ?disconnectivity? in schizophrenia #MMPMID26954593 Coyle JT; Balu D; Puhl M; Konopaske G Harv Rev Psychiatry 2016[Mar]; 24 (2): 80-6 PMID26954593show ga Nearly sixty years ago Seymour Kety proposed that research on genetics and brain pathology but not on neurochemistry would ultimately lead to an understanding of the pathophysiology of schizophrenia. This Perspective will demonstrate how prescient Kety?s proposal was as advances in research on brain structure and on genetics have shaped our current understanding of the pathophysiology of schizophrenia. Brain imaging techniques have shown that schizophrenia is associated with cortical atrophy and ventricular enlargement, which progresses for at least a decade after the onset of psychosis. Cortical atrophy correlates with negative symptoms and cognitive impairment but not with psychosis in schizophrenia. Studies with the Golgi staining technique that illuminates the entire neuron indicate that cortical atrophy was due to reduced synaptic connectivity on the pyramidal neurons and not due to actual loss of neurons. Results of recent genetic studies indicate that several risk genes for schizophrenia are within two degrees of separation from the N-methy-D-aspartate (NMDA) receptor, a subtype of glutamate receptor that is critical to synapse formation and synaptic plasticity. Inactivation of one of these risk genes encoding serine racemase, which synthesizes D-serine, a co-agonist of the NMDA receptor, reproduces the synaptic pathology of schizophrenia. Thus, widespread loss of cortical synaptic connectivity appears to be the primary pathology in schizophrenia that is driven by multiple risk genes that adversely affect synaptogenesis and maintenance as hypothesized by Kety. äA Perspective on the history of the concept of ?disconnectivity? in sc(epmc).pdf DeepDyve Pubget Overpricing