Pathway-based association analysis of genome-wide screening data suggest that genes associated with the γ-aminobutyric acid receptor signaling pathway are involved in neuroleptic-induced, treatment-resistant tardive dyskinesia
OBJECTIVENeuroleptic-induced tardive dyskinesia (TD) is an involuntary movement disorder that develops in patients who have undergone long-term treatment with antipsychotic medications, and its etiology is unclear. In this study, a genome-wide association screening was done to identify the pathway(s...
Gespeichert in:
| Veröffentlicht in: | Pharmacogenetics and genomics 2008-04, Vol.18 (4), p.317-323 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 323 |
|---|---|
| container_issue | 4 |
| container_start_page | 317 |
| container_title | Pharmacogenetics and genomics |
| container_volume | 18 |
| creator | Inada, Toshiya Koga, Minori Ishiguro, Hiroki Horiuchi, Yasue Syu, Aoi Yoshio, Takashi Takahashi, Nagahide Ozaki, Norio Arinami, Tadao |
| description | OBJECTIVENeuroleptic-induced tardive dyskinesia (TD) is an involuntary movement disorder that develops in patients who have undergone long-term treatment with antipsychotic medications, and its etiology is unclear. In this study, a genome-wide association screening was done to identify the pathway(s) in which genetic variations influence susceptibility to neuroleptic-induced TD.
METHODSScreening with Sentrix Human-1 Genotyping BeadChip (Illumina, San Diego, California, USA) was done for 50 Japanese schizophrenia patients with treatment-resistant TD and 50 Japanese schizophrenia patients without TD. A total of 40 573 single nucleotide polymorphisms that were not in linkage disequilibrium with each other and were located in the exonic and intronic regions of 13 307 genes were analyzed. After gene-based corrections, P values for allelic associations were subjected to canonical pathway-based analyses with Ingenuity Pathway Analysis software (Ingenuity Systems, Inc., Redwood City, California, USA).
RESULTSEight genes (ABAT, ALDH9A1, GABRA3, GABRA4, GABRB2, GABRAG3, GPHN, and SLC6A11) contained polymorphisms with gene-based corrected allelic P values of less than 0.05. They were aggregated significantly in 33 genes belonging to the γ-aminobutyric acid (GABA) receptor signaling pathway (P=0.00007, corrected P=0.01). Associations were replicated in an independent sample of 36 patients with TD and 136 patients without TD for polymorphisms in SLC6A11 (GABA transporter 3) (P=0.0004 in the total sample), GABRB2 (β-2 subunit of GABA-A receptor) (P=0.00007 in the total sample), and GABRG3 (γ-3 subunit of GABA-A receptor) (P=0.0006 in the total sample).
CONCLUSIONThe results suggest that the GABA receptor signaling pathway may be involved in genetic susceptibility to treatment-resistant TD, at least in a subgroup of Japanese patients with schizophrenia. The present results suggest that benzodiazepines may be considered as possible treatment option for TD. |
| doi_str_mv | 10.1097/FPC.0b013e3282f70492 |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1097_FPC_0b013e3282f70492</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>18334916</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3805-e83fb3ac0bb68e3e283ee5da566e0b0320742e98e067c77c6b94a6b332dca0f53</originalsourceid><addsrcrecordid>eNpdkc2KFDEUhQtRnHH0DUSycWfGm6R-l9I4Kgw4C10Xt5JbVXGqUk2S6qafy_fwJXwR03TTAy5CAvc75x5ysuytgFsBTfXx7mFzCx0IRUrWsq8gb-Sz7FpUec7Luobnl3clr7JXIfwCUGWTy5fZlaiVyhtRXmd_HzCOezzwDgMZhiEs2mK0i2PocDoEG9jSs4HcMhPfW0MsaE_krBuYwYgsrMNAIbI4YjxyFC4uyXBv45hGxP785jhbt3RrPHirGWprmCdN27h4FuyQth09t6c8DD0x63bLtEsu1jFHq1-mRFvNrTOrJvOBRU8YZ3KRe0pJI7qUA72xO2LmEB5tSmPxdfaixynQm_N9k_28-_xj85Xff__ybfPpnmtVQ8GpVn2nUEPXlTUpkrUiKgwWZUnpo5WEKpfU1ARlpatKl12TY9kpJY1G6At1k-UnX-2XEDz17dbbGf2hFdAeO2tTZ-3_nSXZu5Nsu3YzmSfRuaQEvD8DGDROvUenbbhwEkSTKwVP-_fLFMmHx2ndk29HwimOLQgpFAjBJUANOQDwdKBQ_wCF47i7</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Pathway-based association analysis of genome-wide screening data suggest that genes associated with the γ-aminobutyric acid receptor signaling pathway are involved in neuroleptic-induced, treatment-resistant tardive dyskinesia</title><source>MEDLINE</source><source>Journals@Ovid Complete</source><creator>Inada, Toshiya ; Koga, Minori ; Ishiguro, Hiroki ; Horiuchi, Yasue ; Syu, Aoi ; Yoshio, Takashi ; Takahashi, Nagahide ; Ozaki, Norio ; Arinami, Tadao</creator><creatorcontrib>Inada, Toshiya ; Koga, Minori ; Ishiguro, Hiroki ; Horiuchi, Yasue ; Syu, Aoi ; Yoshio, Takashi ; Takahashi, Nagahide ; Ozaki, Norio ; Arinami, Tadao</creatorcontrib><description>OBJECTIVENeuroleptic-induced tardive dyskinesia (TD) is an involuntary movement disorder that develops in patients who have undergone long-term treatment with antipsychotic medications, and its etiology is unclear. In this study, a genome-wide association screening was done to identify the pathway(s) in which genetic variations influence susceptibility to neuroleptic-induced TD.
METHODSScreening with Sentrix Human-1 Genotyping BeadChip (Illumina, San Diego, California, USA) was done for 50 Japanese schizophrenia patients with treatment-resistant TD and 50 Japanese schizophrenia patients without TD. A total of 40 573 single nucleotide polymorphisms that were not in linkage disequilibrium with each other and were located in the exonic and intronic regions of 13 307 genes were analyzed. After gene-based corrections, P values for allelic associations were subjected to canonical pathway-based analyses with Ingenuity Pathway Analysis software (Ingenuity Systems, Inc., Redwood City, California, USA).
RESULTSEight genes (ABAT, ALDH9A1, GABRA3, GABRA4, GABRB2, GABRAG3, GPHN, and SLC6A11) contained polymorphisms with gene-based corrected allelic P values of less than 0.05. They were aggregated significantly in 33 genes belonging to the γ-aminobutyric acid (GABA) receptor signaling pathway (P=0.00007, corrected P=0.01). Associations were replicated in an independent sample of 36 patients with TD and 136 patients without TD for polymorphisms in SLC6A11 (GABA transporter 3) (P=0.0004 in the total sample), GABRB2 (β-2 subunit of GABA-A receptor) (P=0.00007 in the total sample), and GABRG3 (γ-3 subunit of GABA-A receptor) (P=0.0006 in the total sample).
CONCLUSIONThe results suggest that the GABA receptor signaling pathway may be involved in genetic susceptibility to treatment-resistant TD, at least in a subgroup of Japanese patients with schizophrenia. The present results suggest that benzodiazepines may be considered as possible treatment option for TD.</description><identifier>ISSN: 1744-6872</identifier><identifier>EISSN: 1744-6880</identifier><identifier>DOI: 10.1097/FPC.0b013e3282f70492</identifier><identifier>PMID: 18334916</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>Antipsychotic Agents - adverse effects ; Biological and medical sciences ; Cell physiology ; Cell receptors ; Cell structures and functions ; Dyskinesia, Drug-Induced - genetics ; Dyskinesia, Drug-Induced - metabolism ; Female ; Fundamental and applied biological sciences. Psychology ; General pharmacology ; Genetic Predisposition to Disease ; Genetic Testing ; Genome, Human ; Genotype ; Humans ; Linkage Disequilibrium ; Male ; Medical sciences ; Middle Aged ; Miscellaneous ; Molecular and cellular biology ; Pharmacokinetics. Pharmacogenetics. Drug-receptor interactions ; Pharmacology. Drug treatments ; Polymorphism, Single Nucleotide ; Receptors, GABA - genetics ; Receptors, GABA - metabolism ; Schizophrenia - drug therapy ; Schizophrenia - genetics ; Schizophrenia - metabolism ; Signal Transduction</subject><ispartof>Pharmacogenetics and genomics, 2008-04, Vol.18 (4), p.317-323</ispartof><rights>2008 Lippincott Williams & Wilkins, Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3805-e83fb3ac0bb68e3e283ee5da566e0b0320742e98e067c77c6b94a6b332dca0f53</citedby><cites>FETCH-LOGICAL-c3805-e83fb3ac0bb68e3e283ee5da566e0b0320742e98e067c77c6b94a6b332dca0f53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20194330$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18334916$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Inada, Toshiya</creatorcontrib><creatorcontrib>Koga, Minori</creatorcontrib><creatorcontrib>Ishiguro, Hiroki</creatorcontrib><creatorcontrib>Horiuchi, Yasue</creatorcontrib><creatorcontrib>Syu, Aoi</creatorcontrib><creatorcontrib>Yoshio, Takashi</creatorcontrib><creatorcontrib>Takahashi, Nagahide</creatorcontrib><creatorcontrib>Ozaki, Norio</creatorcontrib><creatorcontrib>Arinami, Tadao</creatorcontrib><title>Pathway-based association analysis of genome-wide screening data suggest that genes associated with the γ-aminobutyric acid receptor signaling pathway are involved in neuroleptic-induced, treatment-resistant tardive dyskinesia</title><title>Pharmacogenetics and genomics</title><addtitle>Pharmacogenet Genomics</addtitle><description>OBJECTIVENeuroleptic-induced tardive dyskinesia (TD) is an involuntary movement disorder that develops in patients who have undergone long-term treatment with antipsychotic medications, and its etiology is unclear. In this study, a genome-wide association screening was done to identify the pathway(s) in which genetic variations influence susceptibility to neuroleptic-induced TD.
METHODSScreening with Sentrix Human-1 Genotyping BeadChip (Illumina, San Diego, California, USA) was done for 50 Japanese schizophrenia patients with treatment-resistant TD and 50 Japanese schizophrenia patients without TD. A total of 40 573 single nucleotide polymorphisms that were not in linkage disequilibrium with each other and were located in the exonic and intronic regions of 13 307 genes were analyzed. After gene-based corrections, P values for allelic associations were subjected to canonical pathway-based analyses with Ingenuity Pathway Analysis software (Ingenuity Systems, Inc., Redwood City, California, USA).
RESULTSEight genes (ABAT, ALDH9A1, GABRA3, GABRA4, GABRB2, GABRAG3, GPHN, and SLC6A11) contained polymorphisms with gene-based corrected allelic P values of less than 0.05. They were aggregated significantly in 33 genes belonging to the γ-aminobutyric acid (GABA) receptor signaling pathway (P=0.00007, corrected P=0.01). Associations were replicated in an independent sample of 36 patients with TD and 136 patients without TD for polymorphisms in SLC6A11 (GABA transporter 3) (P=0.0004 in the total sample), GABRB2 (β-2 subunit of GABA-A receptor) (P=0.00007 in the total sample), and GABRG3 (γ-3 subunit of GABA-A receptor) (P=0.0006 in the total sample).
CONCLUSIONThe results suggest that the GABA receptor signaling pathway may be involved in genetic susceptibility to treatment-resistant TD, at least in a subgroup of Japanese patients with schizophrenia. The present results suggest that benzodiazepines may be considered as possible treatment option for TD.</description><subject>Antipsychotic Agents - adverse effects</subject><subject>Biological and medical sciences</subject><subject>Cell physiology</subject><subject>Cell receptors</subject><subject>Cell structures and functions</subject><subject>Dyskinesia, Drug-Induced - genetics</subject><subject>Dyskinesia, Drug-Induced - metabolism</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>General pharmacology</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic Testing</subject><subject>Genome, Human</subject><subject>Genotype</subject><subject>Humans</subject><subject>Linkage Disequilibrium</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Miscellaneous</subject><subject>Molecular and cellular biology</subject><subject>Pharmacokinetics. Pharmacogenetics. Drug-receptor interactions</subject><subject>Pharmacology. Drug treatments</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Receptors, GABA - genetics</subject><subject>Receptors, GABA - metabolism</subject><subject>Schizophrenia - drug therapy</subject><subject>Schizophrenia - genetics</subject><subject>Schizophrenia - metabolism</subject><subject>Signal Transduction</subject><issn>1744-6872</issn><issn>1744-6880</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc2KFDEUhQtRnHH0DUSycWfGm6R-l9I4Kgw4C10Xt5JbVXGqUk2S6qafy_fwJXwR03TTAy5CAvc75x5ysuytgFsBTfXx7mFzCx0IRUrWsq8gb-Sz7FpUec7Luobnl3clr7JXIfwCUGWTy5fZlaiVyhtRXmd_HzCOezzwDgMZhiEs2mK0i2PocDoEG9jSs4HcMhPfW0MsaE_krBuYwYgsrMNAIbI4YjxyFC4uyXBv45hGxP785jhbt3RrPHirGWprmCdN27h4FuyQth09t6c8DD0x63bLtEsu1jFHq1-mRFvNrTOrJvOBRU8YZ3KRe0pJI7qUA72xO2LmEB5tSmPxdfaixynQm_N9k_28-_xj85Xff__ybfPpnmtVQ8GpVn2nUEPXlTUpkrUiKgwWZUnpo5WEKpfU1ARlpatKl12TY9kpJY1G6At1k-UnX-2XEDz17dbbGf2hFdAeO2tTZ-3_nSXZu5Nsu3YzmSfRuaQEvD8DGDROvUenbbhwEkSTKwVP-_fLFMmHx2ndk29HwimOLQgpFAjBJUANOQDwdKBQ_wCF47i7</recordid><startdate>200804</startdate><enddate>200804</enddate><creator>Inada, Toshiya</creator><creator>Koga, Minori</creator><creator>Ishiguro, Hiroki</creator><creator>Horiuchi, Yasue</creator><creator>Syu, Aoi</creator><creator>Yoshio, Takashi</creator><creator>Takahashi, Nagahide</creator><creator>Ozaki, Norio</creator><creator>Arinami, Tadao</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott Williams and Wilkins</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></search><sort><creationdate>200804</creationdate><title>Pathway-based association analysis of genome-wide screening data suggest that genes associated with the γ-aminobutyric acid receptor signaling pathway are involved in neuroleptic-induced, treatment-resistant tardive dyskinesia</title><author>Inada, Toshiya ; Koga, Minori ; Ishiguro, Hiroki ; Horiuchi, Yasue ; Syu, Aoi ; Yoshio, Takashi ; Takahashi, Nagahide ; Ozaki, Norio ; Arinami, Tadao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3805-e83fb3ac0bb68e3e283ee5da566e0b0320742e98e067c77c6b94a6b332dca0f53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Antipsychotic Agents - adverse effects</topic><topic>Biological and medical sciences</topic><topic>Cell physiology</topic><topic>Cell receptors</topic><topic>Cell structures and functions</topic><topic>Dyskinesia, Drug-Induced - genetics</topic><topic>Dyskinesia, Drug-Induced - metabolism</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>General pharmacology</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic Testing</topic><topic>Genome, Human</topic><topic>Genotype</topic><topic>Humans</topic><topic>Linkage Disequilibrium</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Miscellaneous</topic><topic>Molecular and cellular biology</topic><topic>Pharmacokinetics. Pharmacogenetics. Drug-receptor interactions</topic><topic>Pharmacology. Drug treatments</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Receptors, GABA - genetics</topic><topic>Receptors, GABA - metabolism</topic><topic>Schizophrenia - drug therapy</topic><topic>Schizophrenia - genetics</topic><topic>Schizophrenia - metabolism</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Inada, Toshiya</creatorcontrib><creatorcontrib>Koga, Minori</creatorcontrib><creatorcontrib>Ishiguro, Hiroki</creatorcontrib><creatorcontrib>Horiuchi, Yasue</creatorcontrib><creatorcontrib>Syu, Aoi</creatorcontrib><creatorcontrib>Yoshio, Takashi</creatorcontrib><creatorcontrib>Takahashi, Nagahide</creatorcontrib><creatorcontrib>Ozaki, Norio</creatorcontrib><creatorcontrib>Arinami, Tadao</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><jtitle>Pharmacogenetics and genomics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Inada, Toshiya</au><au>Koga, Minori</au><au>Ishiguro, Hiroki</au><au>Horiuchi, Yasue</au><au>Syu, Aoi</au><au>Yoshio, Takashi</au><au>Takahashi, Nagahide</au><au>Ozaki, Norio</au><au>Arinami, Tadao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pathway-based association analysis of genome-wide screening data suggest that genes associated with the γ-aminobutyric acid receptor signaling pathway are involved in neuroleptic-induced, treatment-resistant tardive dyskinesia</atitle><jtitle>Pharmacogenetics and genomics</jtitle><addtitle>Pharmacogenet Genomics</addtitle><date>2008-04</date><risdate>2008</risdate><volume>18</volume><issue>4</issue><spage>317</spage><epage>323</epage><pages>317-323</pages><issn>1744-6872</issn><eissn>1744-6880</eissn><abstract>OBJECTIVENeuroleptic-induced tardive dyskinesia (TD) is an involuntary movement disorder that develops in patients who have undergone long-term treatment with antipsychotic medications, and its etiology is unclear. In this study, a genome-wide association screening was done to identify the pathway(s) in which genetic variations influence susceptibility to neuroleptic-induced TD.
METHODSScreening with Sentrix Human-1 Genotyping BeadChip (Illumina, San Diego, California, USA) was done for 50 Japanese schizophrenia patients with treatment-resistant TD and 50 Japanese schizophrenia patients without TD. A total of 40 573 single nucleotide polymorphisms that were not in linkage disequilibrium with each other and were located in the exonic and intronic regions of 13 307 genes were analyzed. After gene-based corrections, P values for allelic associations were subjected to canonical pathway-based analyses with Ingenuity Pathway Analysis software (Ingenuity Systems, Inc., Redwood City, California, USA).
RESULTSEight genes (ABAT, ALDH9A1, GABRA3, GABRA4, GABRB2, GABRAG3, GPHN, and SLC6A11) contained polymorphisms with gene-based corrected allelic P values of less than 0.05. They were aggregated significantly in 33 genes belonging to the γ-aminobutyric acid (GABA) receptor signaling pathway (P=0.00007, corrected P=0.01). Associations were replicated in an independent sample of 36 patients with TD and 136 patients without TD for polymorphisms in SLC6A11 (GABA transporter 3) (P=0.0004 in the total sample), GABRB2 (β-2 subunit of GABA-A receptor) (P=0.00007 in the total sample), and GABRG3 (γ-3 subunit of GABA-A receptor) (P=0.0006 in the total sample).
CONCLUSIONThe results suggest that the GABA receptor signaling pathway may be involved in genetic susceptibility to treatment-resistant TD, at least in a subgroup of Japanese patients with schizophrenia. The present results suggest that benzodiazepines may be considered as possible treatment option for TD.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>18334916</pmid><doi>10.1097/FPC.0b013e3282f70492</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1744-6872 |
| ispartof | Pharmacogenetics and genomics, 2008-04, Vol.18 (4), p.317-323 |
| issn | 1744-6872 1744-6880 |
| language | eng |
| recordid | cdi_crossref_primary_10_1097_FPC_0b013e3282f70492 |
| source | MEDLINE; Journals@Ovid Complete |
| subjects | Antipsychotic Agents - adverse effects Biological and medical sciences Cell physiology Cell receptors Cell structures and functions Dyskinesia, Drug-Induced - genetics Dyskinesia, Drug-Induced - metabolism Female Fundamental and applied biological sciences. Psychology General pharmacology Genetic Predisposition to Disease Genetic Testing Genome, Human Genotype Humans Linkage Disequilibrium Male Medical sciences Middle Aged Miscellaneous Molecular and cellular biology Pharmacokinetics. Pharmacogenetics. Drug-receptor interactions Pharmacology. Drug treatments Polymorphism, Single Nucleotide Receptors, GABA - genetics Receptors, GABA - metabolism Schizophrenia - drug therapy Schizophrenia - genetics Schizophrenia - metabolism Signal Transduction |
| title | Pathway-based association analysis of genome-wide screening data suggest that genes associated with the γ-aminobutyric acid receptor signaling pathway are involved in neuroleptic-induced, treatment-resistant tardive dyskinesia |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-04T05%3A23%3A04IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmed_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Pathway-based%20association%20analysis%20of%20genome-wide%20screening%20data%20suggest%20that%20genes%20associated%20with%20the%20%CE%B3-aminobutyric%20acid%20receptor%20signaling%20pathway%20are%20involved%20in%20neuroleptic-induced,%20treatment-resistant%20tardive%20dyskinesia&rft.jtitle=Pharmacogenetics%20and%20genomics&rft.au=Inada,%20Toshiya&rft.date=2008-04&rft.volume=18&rft.issue=4&rft.spage=317&rft.epage=323&rft.pages=317-323&rft.issn=1744-6872&rft.eissn=1744-6880&rft_id=info:doi/10.1097/FPC.0b013e3282f70492&rft_dat=%3Cpubmed_cross%3E18334916%3C/pubmed_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/18334916&rfr_iscdi=true |