Differential regional N -acetylaspartate deficits in postmortem brain in schizophrenia, bipolar disorder and major depressive disorder
Abstract There is substantial evidence for the involvement of the hippocampus and subcortical regions in the neuropathology of schizophrenia. Deficits of N -acetylaspartate (NAA) have been found in schizophrenia and bipolar disorder which may reflect neuronal loss and/or dysfunction. N -acetylaspart...
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| Veröffentlicht in: | Journal of psychiatric research 2011-01, Vol.45 (1), p.54-59 |
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| creator | Reynolds, Lindsay M Reynolds, Gavin P |
| description | Abstract There is substantial evidence for the involvement of the hippocampus and subcortical regions in the neuropathology of schizophrenia. Deficits of N -acetylaspartate (NAA) have been found in schizophrenia and bipolar disorder which may reflect neuronal loss and/or dysfunction. N -acetylaspartylglutamate (NAAG) is the most abundant peptide transmitter in the mammalian nervous system. It is an agonist at presynaptic metabotropic glutamate receptors mGluR3, inhibiting glutamate release. NAA and NAAG and were measured in hippocampal, striatal, amygdala and cingulate gyrus regions of human postmortem tissue from controls and subjects with schizophrenia, bipolar disorder and major depressive disorder. There are significant deficits in hippocampal NAA concentrations in all patient groups. In the amygdala there are significant NAA deficits in schizophrenia and depression and significant deficits of NAAG in the amygdala in the depression group. The deficits in NAA reported in this study confirm the importance of hippocampal and other subcortical structures in the neuropathology of the major psychiatric disorders. |
| doi_str_mv | 10.1016/j.jpsychires.2010.05.001 |
| format | Article |
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Deficits of N -acetylaspartate (NAA) have been found in schizophrenia and bipolar disorder which may reflect neuronal loss and/or dysfunction. N -acetylaspartylglutamate (NAAG) is the most abundant peptide transmitter in the mammalian nervous system. It is an agonist at presynaptic metabotropic glutamate receptors mGluR3, inhibiting glutamate release. NAA and NAAG and were measured in hippocampal, striatal, amygdala and cingulate gyrus regions of human postmortem tissue from controls and subjects with schizophrenia, bipolar disorder and major depressive disorder. There are significant deficits in hippocampal NAA concentrations in all patient groups. In the amygdala there are significant NAA deficits in schizophrenia and depression and significant deficits of NAAG in the amygdala in the depression group. The deficits in NAA reported in this study confirm the importance of hippocampal and other subcortical structures in the neuropathology of the major psychiatric disorders.</description><identifier>ISSN: 0022-3956</identifier><identifier>EISSN: 1879-1379</identifier><identifier>DOI: 10.1016/j.jpsychires.2010.05.001</identifier><identifier>PMID: 20684832</identifier><identifier>CODEN: JPYRA3</identifier><language>eng</language><publisher>Kidlington: Elsevier Ltd</publisher><subject>Adult ; Adult and adolescent clinical studies ; Aspartic Acid - analogs & derivatives ; Aspartic Acid - metabolism ; Biological and medical sciences ; Bipolar affective disorder ; Bipolar disorder ; Bipolar Disorder - pathology ; Bipolar disorders ; Brain - metabolism ; Brain - pathology ; Depression ; Depressive Disorder, Major - pathology ; Depressive personality disorders ; Dipeptides - metabolism ; Female ; Frozen brain sections ; Humans ; Indexing in process ; Major depressive disorder ; Male ; Medical sciences ; Middle Aged ; Mood disorders ; N-acetylaspartate ; N-acetylaspartylglutamate ; Nervous system ; Neuropathology ; Postmortems ; Psychiatry ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Psychoses ; Schizophrenia ; Schizophrenia - pathology</subject><ispartof>Journal of psychiatric research, 2011-01, Vol.45 (1), p.54-59</ispartof><rights>Elsevier Ltd</rights><rights>2010 Elsevier Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2010 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c589t-fccbdd0c7a54463aefaf45d122a980bd4833ece4b9ed5f5b7090d96e43d7aaa73</citedby><cites>FETCH-LOGICAL-c589t-fccbdd0c7a54463aefaf45d122a980bd4833ece4b9ed5f5b7090d96e43d7aaa73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0022395610001433$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,30977,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23794652$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20684832$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reynolds, Lindsay M</creatorcontrib><creatorcontrib>Reynolds, Gavin P</creatorcontrib><title>Differential regional N -acetylaspartate deficits in postmortem brain in schizophrenia, bipolar disorder and major depressive disorder</title><title>Journal of psychiatric research</title><addtitle>J Psychiatr Res</addtitle><description>Abstract There is substantial evidence for the involvement of the hippocampus and subcortical regions in the neuropathology of schizophrenia. Deficits of N -acetylaspartate (NAA) have been found in schizophrenia and bipolar disorder which may reflect neuronal loss and/or dysfunction. N -acetylaspartylglutamate (NAAG) is the most abundant peptide transmitter in the mammalian nervous system. It is an agonist at presynaptic metabotropic glutamate receptors mGluR3, inhibiting glutamate release. NAA and NAAG and were measured in hippocampal, striatal, amygdala and cingulate gyrus regions of human postmortem tissue from controls and subjects with schizophrenia, bipolar disorder and major depressive disorder. There are significant deficits in hippocampal NAA concentrations in all patient groups. In the amygdala there are significant NAA deficits in schizophrenia and depression and significant deficits of NAAG in the amygdala in the depression group. The deficits in NAA reported in this study confirm the importance of hippocampal and other subcortical structures in the neuropathology of the major psychiatric disorders.</description><subject>Adult</subject><subject>Adult and adolescent clinical studies</subject><subject>Aspartic Acid - analogs & derivatives</subject><subject>Aspartic Acid - metabolism</subject><subject>Biological and medical sciences</subject><subject>Bipolar affective disorder</subject><subject>Bipolar disorder</subject><subject>Bipolar Disorder - pathology</subject><subject>Bipolar disorders</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Depression</subject><subject>Depressive Disorder, Major - pathology</subject><subject>Depressive personality disorders</subject><subject>Dipeptides - metabolism</subject><subject>Female</subject><subject>Frozen brain sections</subject><subject>Humans</subject><subject>Indexing in process</subject><subject>Major depressive disorder</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mood disorders</subject><subject>N-acetylaspartate</subject><subject>N-acetylaspartylglutamate</subject><subject>Nervous system</subject><subject>Neuropathology</subject><subject>Postmortems</subject><subject>Psychiatry</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Psychoses</subject><subject>Schizophrenia</subject><subject>Schizophrenia - pathology</subject><issn>0022-3956</issn><issn>1879-1379</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>7QJ</sourceid><recordid>eNqNkttu1DAQhi0EotuFV0C-QXDRLD7mcIME5ShVcAFcWxN7Qh2SOLWzlZYH4LnxsksrcQFIlm2NP8-M_f-EUM42nPHyWb_p57Szlz5i2giWw0xvGON3yIrXVVNwWTV3yYoxIQrZ6PKEnKbUM8YqwdV9ciJYWataihX58cp3HUacFg8DjfjVhylvPtACLC67AdIMcYEFqcPOW78k6ic6h7SMIS440jZCDuSRcjvfw3yZc3k4o62fwwCROp9CdBgpTI6O0Iccwjn3nfw13pw-IPc6GBI-PK5r8uXN68_n74qLj2_fn7-4KKyum6XorG2dY7YCrVQpATvolHZcCGhq1rr8JokWVdug051uK9Yw15SopKsAoJJr8uSQd47haotpMaNPFocBJgzbZOpS6EYoXf-blJXSqvxFPv0rybnQQkqVpzWpD6iNIaWInZmjHyHuDGdmr6zpza2yZq-sYdpkZfPVR8cq23ZEd3Pxt5QZeHwEIFkYugiT9emWy5bI7e65lwcO8z9fe4wmWY-TRZdr2sW44P-nm-d_JLGDn3yu-w13mPqwjdlG-e0mCcPMp70T90bk2YNcSSl_Ag9J31k</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>Reynolds, Lindsay M</creator><creator>Reynolds, Gavin P</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope><scope>7QJ</scope></search><sort><creationdate>20110101</creationdate><title>Differential regional N -acetylaspartate deficits in postmortem brain in schizophrenia, bipolar disorder and major depressive disorder</title><author>Reynolds, Lindsay M ; Reynolds, Gavin P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c589t-fccbdd0c7a54463aefaf45d122a980bd4833ece4b9ed5f5b7090d96e43d7aaa73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adult</topic><topic>Adult and adolescent clinical studies</topic><topic>Aspartic Acid - analogs & derivatives</topic><topic>Aspartic Acid - metabolism</topic><topic>Biological and medical sciences</topic><topic>Bipolar affective disorder</topic><topic>Bipolar disorder</topic><topic>Bipolar Disorder - pathology</topic><topic>Bipolar disorders</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Depression</topic><topic>Depressive Disorder, Major - pathology</topic><topic>Depressive personality disorders</topic><topic>Dipeptides - metabolism</topic><topic>Female</topic><topic>Frozen brain sections</topic><topic>Humans</topic><topic>Indexing in process</topic><topic>Major depressive disorder</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mood disorders</topic><topic>N-acetylaspartate</topic><topic>N-acetylaspartylglutamate</topic><topic>Nervous system</topic><topic>Neuropathology</topic><topic>Postmortems</topic><topic>Psychiatry</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Psychoses</topic><topic>Schizophrenia</topic><topic>Schizophrenia - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Reynolds, Lindsay M</creatorcontrib><creatorcontrib>Reynolds, Gavin P</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Applied Social Sciences Index & Abstracts (ASSIA)</collection><jtitle>Journal of psychiatric research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Reynolds, Lindsay M</au><au>Reynolds, Gavin P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential regional N -acetylaspartate deficits in postmortem brain in schizophrenia, bipolar disorder and major depressive disorder</atitle><jtitle>Journal of psychiatric research</jtitle><addtitle>J Psychiatr Res</addtitle><date>2011-01-01</date><risdate>2011</risdate><volume>45</volume><issue>1</issue><spage>54</spage><epage>59</epage><pages>54-59</pages><issn>0022-3956</issn><eissn>1879-1379</eissn><coden>JPYRA3</coden><abstract>Abstract There is substantial evidence for the involvement of the hippocampus and subcortical regions in the neuropathology of schizophrenia. Deficits of N -acetylaspartate (NAA) have been found in schizophrenia and bipolar disorder which may reflect neuronal loss and/or dysfunction. N -acetylaspartylglutamate (NAAG) is the most abundant peptide transmitter in the mammalian nervous system. It is an agonist at presynaptic metabotropic glutamate receptors mGluR3, inhibiting glutamate release. NAA and NAAG and were measured in hippocampal, striatal, amygdala and cingulate gyrus regions of human postmortem tissue from controls and subjects with schizophrenia, bipolar disorder and major depressive disorder. There are significant deficits in hippocampal NAA concentrations in all patient groups. In the amygdala there are significant NAA deficits in schizophrenia and depression and significant deficits of NAAG in the amygdala in the depression group. The deficits in NAA reported in this study confirm the importance of hippocampal and other subcortical structures in the neuropathology of the major psychiatric disorders.</abstract><cop>Kidlington</cop><pub>Elsevier Ltd</pub><pmid>20684832</pmid><doi>10.1016/j.jpsychires.2010.05.001</doi><tpages>6</tpages></addata></record> |
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| subjects | Adult Adult and adolescent clinical studies Aspartic Acid - analogs & derivatives Aspartic Acid - metabolism Biological and medical sciences Bipolar affective disorder Bipolar disorder Bipolar Disorder - pathology Bipolar disorders Brain - metabolism Brain - pathology Depression Depressive Disorder, Major - pathology Depressive personality disorders Dipeptides - metabolism Female Frozen brain sections Humans Indexing in process Major depressive disorder Male Medical sciences Middle Aged Mood disorders N-acetylaspartate N-acetylaspartylglutamate Nervous system Neuropathology Postmortems Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Schizophrenia Schizophrenia - pathology |
| title | Differential regional N -acetylaspartate deficits in postmortem brain in schizophrenia, bipolar disorder and major depressive disorder |
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