Brain-derived neurotrophic factor G196A polymorphism and clinical features in Parkinson's disease

Gao L, Díaz‐Corrales FJ, Carrillo F, Díaz‐Martín J, Caceres‐Redondo MT, Carballo M, Palomino A, López‐Barneo J, Mir P. Brain‐derived neurotrophic factor G196A polymorphism and clinical features in Parkinson’s disease.
Acta Neurol Scand: 2010: 122: 41–45.
© 2010 The Authors Journal compilation © 2010...

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Veröffentlicht in:Acta neurologica Scandinavica 2010-07, Vol.122 (1), p.41-45
Hauptverfasser: Gao, L., Díaz-Corrales, F. J., Carrillo, F., Díaz-Martín, J., Caceres-Redondo, M. T., Carballo, M., Palomino, A., López-Barneo, J., Mir, P.
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container_issue 1
container_start_page 41
container_title Acta neurologica Scandinavica
container_volume 122
creator Gao, L.
Díaz-Corrales, F. J.
Carrillo, F.
Díaz-Martín, J.
Caceres-Redondo, M. T.
Carballo, M.
Palomino, A.
López-Barneo, J.
Mir, P.
description Gao L, Díaz‐Corrales FJ, Carrillo F, Díaz‐Martín J, Caceres‐Redondo MT, Carballo M, Palomino A, López‐Barneo J, Mir P. Brain‐derived neurotrophic factor G196A polymorphism and clinical features in Parkinson’s disease.
Acta Neurol Scand: 2010: 122: 41–45.
© 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. Objectives –  Parkinson’s disease (PD) is characterized by the dopaminergic neuronal death in substantia nigra, and genetic factors appear to be involved in the pathophysiology of this disease. Brain‐derived neurotrophic factor (BDNF) is widely expressed in the central nervous system and is necessary for the survival of dopaminergic neurons in substantia nigra. G196A, a common polymorphism of the BDNF gene, not only affects cognitive and motor processes, but also is associated with various psychiatric disorders. We evaluated whether G196A polymorphism is associated with PD and/or modifies clinical manifestations in PD patients. Methods –  We included 193 PD patients and 300 control subjects. G196A polymorphism was screened by restriction fragment length polymorphism analysis. Clinical features of each patient were examined in detail. The possible association between genotype and clinical characteristics were determined by bivariate and multivariate analyses. Results –  The distribution of G196A allele and genotype frequency was similar between PD and control subjects. Clinical characteristics, including Hoehn‐Yahr stage, motor symptoms, non‐motor symptoms (depression, cognitive dysfunction, psychiatric dysfunctions, and sleep behavior disorder), and dyskinesias, were not associated with this polymorphism. Conclusions –  G196A polymorphism is not a risk factor for PD and does not seem to modify clinical features in PD patients studied here.
doi_str_mv 10.1111/j.1600-0404.2009.01253.x
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Acta Neurol Scand: 2010: 122: 41–45.
© 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. Objectives –  Parkinson’s disease (PD) is characterized by the dopaminergic neuronal death in substantia nigra, and genetic factors appear to be involved in the pathophysiology of this disease. Brain‐derived neurotrophic factor (BDNF) is widely expressed in the central nervous system and is necessary for the survival of dopaminergic neurons in substantia nigra. G196A, a common polymorphism of the BDNF gene, not only affects cognitive and motor processes, but also is associated with various psychiatric disorders. We evaluated whether G196A polymorphism is associated with PD and/or modifies clinical manifestations in PD patients. Methods –  We included 193 PD patients and 300 control subjects. G196A polymorphism was screened by restriction fragment length polymorphism analysis. Clinical features of each patient were examined in detail. The possible association between genotype and clinical characteristics were determined by bivariate and multivariate analyses. Results –  The distribution of G196A allele and genotype frequency was similar between PD and control subjects. Clinical characteristics, including Hoehn‐Yahr stage, motor symptoms, non‐motor symptoms (depression, cognitive dysfunction, psychiatric dysfunctions, and sleep behavior disorder), and dyskinesias, were not associated with this polymorphism. Conclusions –  G196A polymorphism is not a risk factor for PD and does not seem to modify clinical features in PD patients studied here.</description><identifier>ISSN: 0001-6314</identifier><identifier>EISSN: 1600-0404</identifier><identifier>DOI: 10.1111/j.1600-0404.2009.01253.x</identifier><identifier>PMID: 20085561</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Aged ; BDNF G196A polymorphism ; Brain-Derived Neurotrophic Factor - genetics ; Case-Control Studies ; clinical manifestation ; Female ; Genotype ; Humans ; Male ; Middle Aged ; Multivariate Analysis ; Parkinson Disease - genetics ; Parkinson Disease - physiopathology ; Parkinson's disease ; Polymorphism, Restriction Fragment Length ; risk factor</subject><ispartof>Acta neurologica Scandinavica, 2010-07, Vol.122 (1), p.41-45</ispartof><rights>Copyright © 2010 The Authors. Journal compilation © 2010 Blackwell Munksgaard</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4393-c9ef3e5b49ee9d4dd1592712f35f2332e5aa7e6e9c2890e49fde04b8f39ea2333</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1600-0404.2009.01253.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1600-0404.2009.01253.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20085561$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gao, L.</creatorcontrib><creatorcontrib>Díaz-Corrales, F. J.</creatorcontrib><creatorcontrib>Carrillo, F.</creatorcontrib><creatorcontrib>Díaz-Martín, J.</creatorcontrib><creatorcontrib>Caceres-Redondo, M. T.</creatorcontrib><creatorcontrib>Carballo, M.</creatorcontrib><creatorcontrib>Palomino, A.</creatorcontrib><creatorcontrib>López-Barneo, J.</creatorcontrib><creatorcontrib>Mir, P.</creatorcontrib><title>Brain-derived neurotrophic factor G196A polymorphism and clinical features in Parkinson's disease</title><title>Acta neurologica Scandinavica</title><addtitle>Acta Neurol Scand</addtitle><description>Gao L, Díaz‐Corrales FJ, Carrillo F, Díaz‐Martín J, Caceres‐Redondo MT, Carballo M, Palomino A, López‐Barneo J, Mir P. Brain‐derived neurotrophic factor G196A polymorphism and clinical features in Parkinson’s disease.
Acta Neurol Scand: 2010: 122: 41–45.
© 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. Objectives –  Parkinson’s disease (PD) is characterized by the dopaminergic neuronal death in substantia nigra, and genetic factors appear to be involved in the pathophysiology of this disease. Brain‐derived neurotrophic factor (BDNF) is widely expressed in the central nervous system and is necessary for the survival of dopaminergic neurons in substantia nigra. G196A, a common polymorphism of the BDNF gene, not only affects cognitive and motor processes, but also is associated with various psychiatric disorders. We evaluated whether G196A polymorphism is associated with PD and/or modifies clinical manifestations in PD patients. Methods –  We included 193 PD patients and 300 control subjects. G196A polymorphism was screened by restriction fragment length polymorphism analysis. Clinical features of each patient were examined in detail. The possible association between genotype and clinical characteristics were determined by bivariate and multivariate analyses. Results –  The distribution of G196A allele and genotype frequency was similar between PD and control subjects. Clinical characteristics, including Hoehn‐Yahr stage, motor symptoms, non‐motor symptoms (depression, cognitive dysfunction, psychiatric dysfunctions, and sleep behavior disorder), and dyskinesias, were not associated with this polymorphism. Conclusions –  G196A polymorphism is not a risk factor for PD and does not seem to modify clinical features in PD patients studied here.</description><subject>Aged</subject><subject>BDNF G196A polymorphism</subject><subject>Brain-Derived Neurotrophic Factor - genetics</subject><subject>Case-Control Studies</subject><subject>clinical manifestation</subject><subject>Female</subject><subject>Genotype</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Multivariate Analysis</subject><subject>Parkinson Disease - genetics</subject><subject>Parkinson Disease - physiopathology</subject><subject>Parkinson's disease</subject><subject>Polymorphism, Restriction Fragment Length</subject><subject>risk factor</subject><issn>0001-6314</issn><issn>1600-0404</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1OGzEUhS1URAL0FSrvsprBf-MZL7pIA6SVIFQq0KXljO-oTucntWdK8vZ4Gpo13tjW-b67uAchTElK47napFQSkhBBRMoIUSmhLOPp7gRNj8EHNCWE0ERyKiboPIRN_LFciDM0iU6RZZJOkfnijWsTC979BYtbGHzX-277y5W4MmXfebykSs7xtqv3TedjEBpsWovL2rWuNDWuwPSDh4Bdi78b_9u1oWtnAVsXwAS4RKeVqQN8fLsv0NPtzePia3L3sPy2mN8lpeCKJ6WCikO2FgpAWWEtzRTLKat4VjHOGWTG5CBBlaxQBISqLBCxLiquwESAX6DZYe7Wd38GCL1uXCihrk0L3RB0LiTJlWTvIDmXTBWsiOSnN3JYN2D11rvG-L3-v78IfD4AL66G_TGnRI896Y0e69BjHaOj9L-e9E7PVzfjK_rJwXehh93Rj1vUMud5pn-ulprdXz__uL6nWvFXcOGVCA</recordid><startdate>201007</startdate><enddate>201007</enddate><creator>Gao, L.</creator><creator>Díaz-Corrales, F. J.</creator><creator>Carrillo, F.</creator><creator>Díaz-Martín, J.</creator><creator>Caceres-Redondo, M. T.</creator><creator>Carballo, M.</creator><creator>Palomino, A.</creator><creator>López-Barneo, J.</creator><creator>Mir, P.</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>201007</creationdate><title>Brain-derived neurotrophic factor G196A polymorphism and clinical features in Parkinson's disease</title><author>Gao, L. ; Díaz-Corrales, F. J. ; Carrillo, F. ; Díaz-Martín, J. ; Caceres-Redondo, M. T. ; Carballo, M. ; Palomino, A. ; López-Barneo, J. ; Mir, P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4393-c9ef3e5b49ee9d4dd1592712f35f2332e5aa7e6e9c2890e49fde04b8f39ea2333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Aged</topic><topic>BDNF G196A polymorphism</topic><topic>Brain-Derived Neurotrophic Factor - genetics</topic><topic>Case-Control Studies</topic><topic>clinical manifestation</topic><topic>Female</topic><topic>Genotype</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Multivariate Analysis</topic><topic>Parkinson Disease - genetics</topic><topic>Parkinson Disease - physiopathology</topic><topic>Parkinson's disease</topic><topic>Polymorphism, Restriction Fragment Length</topic><topic>risk factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gao, L.</creatorcontrib><creatorcontrib>Díaz-Corrales, F. J.</creatorcontrib><creatorcontrib>Carrillo, F.</creatorcontrib><creatorcontrib>Díaz-Martín, J.</creatorcontrib><creatorcontrib>Caceres-Redondo, M. T.</creatorcontrib><creatorcontrib>Carballo, M.</creatorcontrib><creatorcontrib>Palomino, A.</creatorcontrib><creatorcontrib>López-Barneo, J.</creatorcontrib><creatorcontrib>Mir, P.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Acta neurologica Scandinavica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gao, L.</au><au>Díaz-Corrales, F. J.</au><au>Carrillo, F.</au><au>Díaz-Martín, J.</au><au>Caceres-Redondo, M. T.</au><au>Carballo, M.</au><au>Palomino, A.</au><au>López-Barneo, J.</au><au>Mir, P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Brain-derived neurotrophic factor G196A polymorphism and clinical features in Parkinson's disease</atitle><jtitle>Acta neurologica Scandinavica</jtitle><addtitle>Acta Neurol Scand</addtitle><date>2010-07</date><risdate>2010</risdate><volume>122</volume><issue>1</issue><spage>41</spage><epage>45</epage><pages>41-45</pages><issn>0001-6314</issn><eissn>1600-0404</eissn><abstract>Gao L, Díaz‐Corrales FJ, Carrillo F, Díaz‐Martín J, Caceres‐Redondo MT, Carballo M, Palomino A, López‐Barneo J, Mir P. Brain‐derived neurotrophic factor G196A polymorphism and clinical features in Parkinson’s disease.
Acta Neurol Scand: 2010: 122: 41–45.
© 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. Objectives –  Parkinson’s disease (PD) is characterized by the dopaminergic neuronal death in substantia nigra, and genetic factors appear to be involved in the pathophysiology of this disease. Brain‐derived neurotrophic factor (BDNF) is widely expressed in the central nervous system and is necessary for the survival of dopaminergic neurons in substantia nigra. G196A, a common polymorphism of the BDNF gene, not only affects cognitive and motor processes, but also is associated with various psychiatric disorders. We evaluated whether G196A polymorphism is associated with PD and/or modifies clinical manifestations in PD patients. Methods –  We included 193 PD patients and 300 control subjects. G196A polymorphism was screened by restriction fragment length polymorphism analysis. Clinical features of each patient were examined in detail. The possible association between genotype and clinical characteristics were determined by bivariate and multivariate analyses. Results –  The distribution of G196A allele and genotype frequency was similar between PD and control subjects. Clinical characteristics, including Hoehn‐Yahr stage, motor symptoms, non‐motor symptoms (depression, cognitive dysfunction, psychiatric dysfunctions, and sleep behavior disorder), and dyskinesias, were not associated with this polymorphism. Conclusions –  G196A polymorphism is not a risk factor for PD and does not seem to modify clinical features in PD patients studied here.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20085561</pmid><doi>10.1111/j.1600-0404.2009.01253.x</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record>
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subjects Aged
BDNF G196A polymorphism
Brain-Derived Neurotrophic Factor - genetics
Case-Control Studies
clinical manifestation
Female
Genotype
Humans
Male
Middle Aged
Multivariate Analysis
Parkinson Disease - genetics
Parkinson Disease - physiopathology
Parkinson's disease
Polymorphism, Restriction Fragment Length
risk factor
title Brain-derived neurotrophic factor G196A polymorphism and clinical features in Parkinson's disease
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