Aldehyde dehydrogenase variation enhances effect of pesticides associated with Parkinson disease
Identifieur interne : 000039 ( PascalFrancis/Corpus ); précédent : 000038; suivant : 000040Aldehyde dehydrogenase variation enhances effect of pesticides associated with Parkinson disease
Auteurs : Arthur G. Fitzmaurice ; Shannon L. Rhodes ; Myles Cockburn ; Beate Ritz ; Jeff M. BronsteinSource :
- Neurology [ 0028-3878 ] ; 2014.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
Objective: The objective of this study was to determine whether environmental and genetic alterations of neuronal aldehyde dehydrogenase (ALDH) enzymes were associated with increased Parkinson disease (PD) risk in an epidemiologic study. Methods: A novel ex vivo assay was developed to identify pesticides that can inhibit neuronal ALDH activity. These were investigated for PD associations in a population-based case-control study, the Parkinson's Environment & Genes (PEG) Study. Common variants in the mitochondrial ALDH2 gene were genotyped to assess effect measure modification (statistical interaction) of the pesticide effects by genetic variation. Results: All of the metal-coordinating dithiocarbamates tested (e.g., maneb, ziram), 2 imidazoles (benomyl, triflumizole), 2 dicarboxymides (captan, folpet), and 1 organochlorine (dieldrin) inhibited ALDH activity, potentially via metabolic byproducts (e.g., carbon disulfide, thiophosgene). Fifteen screened pesticides did not inhibit ALDH. Exposures to ALDH-inhibiting pesticides were associated with 2- to 6-fold increases in PD risk; genetic variation in ALDH2 exacerbated PD risk in subjects exposed to ALDH-inhibiting pesticides. Conclusion: ALDH inhibition appears to be an important mechanism through which environmental toxicants contribute to PD pathogenesis, especially in genetically vulnerable individuals, suggesting several potential interventions to reduce PD occurrence or slow or reverse its progression.
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Format Inist (serveur)
| NO : | PASCAL 14-0057226 INIST |
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| ET : | Aldehyde dehydrogenase variation enhances effect of pesticides associated with Parkinson disease |
| AU : | FITZMAURICE (Arthur G.); RHODES (Shannon L.); COCKBURN (Myles); RITZ (Beate); BRONSTEIN (Jeff M.) |
| AF : | Department of Neurology, David Geffen School of Medicine at UCLA/Los Angeles/Etats-Unis (1 aut., 4 aut., 5 aut.); Department of Molecular Toxicology, University of California/Los Angeles/Etats-Unis (1 aut., 4 aut., 5 aut.); Department of Epidemiology, UCLA Fielding School of Public Health/Los Angeles/Etats-Unis (2 aut., 4 aut.); Department of Environmental Health Sciences, UCLA Fielding School of Public Health/Los Angeles/Etats-Unis (4 aut.); Department of Preventive Medicine, Keck School of Medicine of USC/Los Angeles/Etats-Unis (3 aut.); Parkinson's Disease Research, Education, and Clinical Center, Greater Los Angeles Veterans Affairs Medical Center/Los Angeles/Canada (5 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Neurology; ISSN 0028-3878; Coden NEURAI; Etats-Unis; Da. 2014; Vol. 82; No. 5; Pp. 419-426; Bibl. 40 ref. |
| LA : | Anglais |
| EA : | Objective: The objective of this study was to determine whether environmental and genetic alterations of neuronal aldehyde dehydrogenase (ALDH) enzymes were associated with increased Parkinson disease (PD) risk in an epidemiologic study. Methods: A novel ex vivo assay was developed to identify pesticides that can inhibit neuronal ALDH activity. These were investigated for PD associations in a population-based case-control study, the Parkinson's Environment & Genes (PEG) Study. Common variants in the mitochondrial ALDH2 gene were genotyped to assess effect measure modification (statistical interaction) of the pesticide effects by genetic variation. Results: All of the metal-coordinating dithiocarbamates tested (e.g., maneb, ziram), 2 imidazoles (benomyl, triflumizole), 2 dicarboxymides (captan, folpet), and 1 organochlorine (dieldrin) inhibited ALDH activity, potentially via metabolic byproducts (e.g., carbon disulfide, thiophosgene). Fifteen screened pesticides did not inhibit ALDH. Exposures to ALDH-inhibiting pesticides were associated with 2- to 6-fold increases in PD risk; genetic variation in ALDH2 exacerbated PD risk in subjects exposed to ALDH-inhibiting pesticides. Conclusion: ALDH inhibition appears to be an important mechanism through which environmental toxicants contribute to PD pathogenesis, especially in genetically vulnerable individuals, suggesting several potential interventions to reduce PD occurrence or slow or reverse its progression. |
| CC : | 002B17G; 002B17A01; 002B17A03 |
| FD : | Maladie de Parkinson; Pathologie du système nerveux; Aldehyde dehydrogenase (NAD+); Pesticide |
| FG : | Oxidoreductases; Enzyme; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central |
| ED : | Parkinson disease; Nervous system diseases; Aldehyde dehydrogenase (NAD+); Pesticides |
| EG : | Oxidoreductases; Enzyme; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease |
| SD : | Parkinson enfermedad; Sistema nervioso patología; Aldehyde dehydrogenase (NAD+); Plaguicida |
| LO : | INIST-6345.354000501695730100 |
| ID : | 14-0057226 |
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Bronstein</name><affiliation><inist:fA14 i1="01"><s1>Department of Neurology, David Geffen School of Medicine at UCLA</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Molecular Toxicology, University of California</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="06"><s1>Parkinson's Disease Research, Education, and Clinical Center, Greater Los Angeles Veterans Affairs Medical Center</s1><s2>Los Angeles</s2><s3>CAN</s3><sZ>5 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">14-0057226</idno><date when="2014">2014</date><idno type="stanalyst">PASCAL 14-0057226 INIST</idno><idno type="RBID">Pascal:14-0057226</idno><idno type="wicri:Area/PascalFrancis/Corpus">000039</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Aldehyde dehydrogenase variation enhances effect of pesticides associated with Parkinson disease</title><author><name sortKey="Fitzmaurice, Arthur G" sort="Fitzmaurice, Arthur G" uniqKey="Fitzmaurice A" first="Arthur G." last="Fitzmaurice">Arthur G. Fitzmaurice</name><affiliation><inist:fA14 i1="01"><s1>Department of Neurology, David Geffen School of Medicine at UCLA</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Molecular Toxicology, University of California</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Rhodes, Shannon L" sort="Rhodes, Shannon L" uniqKey="Rhodes S" first="Shannon L." last="Rhodes">Shannon L. Rhodes</name><affiliation><inist:fA14 i1="03"><s1>Department of Epidemiology, UCLA Fielding School of Public Health</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Cockburn, Myles" sort="Cockburn, Myles" uniqKey="Cockburn M" first="Myles" last="Cockburn">Myles Cockburn</name><affiliation><inist:fA14 i1="05"><s1>Department of Preventive Medicine, Keck School of Medicine of USC</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>3 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ritz, Beate" sort="Ritz, Beate" uniqKey="Ritz B" first="Beate" last="Ritz">Beate Ritz</name><affiliation><inist:fA14 i1="01"><s1>Department of Neurology, David Geffen School of Medicine at UCLA</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Molecular Toxicology, University of California</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Department of Epidemiology, UCLA Fielding School of Public Health</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Department of Environmental Health Sciences, UCLA Fielding School of Public Health</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Bronstein, Jeff M" sort="Bronstein, Jeff M" uniqKey="Bronstein J" first="Jeff M." last="Bronstein">Jeff M. Bronstein</name><affiliation><inist:fA14 i1="01"><s1>Department of Neurology, David Geffen School of Medicine at UCLA</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Molecular Toxicology, University of California</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="06"><s1>Parkinson's Disease Research, Education, and Clinical Center, Greater Los Angeles Veterans Affairs Medical Center</s1><s2>Los Angeles</s2><s3>CAN</s3><sZ>5 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Neurology</title><title level="j" type="abbreviated">Neurology</title><idno type="ISSN">0028-3878</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Neurology</title><title level="j" type="abbreviated">Neurology</title><idno type="ISSN">0028-3878</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Nervous system diseases</term><term>Parkinson disease</term><term>Pesticides</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Pesticide</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective: The objective of this study was to determine whether environmental and genetic alterations of neuronal aldehyde dehydrogenase (ALDH) enzymes were associated with increased Parkinson disease (PD) risk in an epidemiologic study. Methods: A novel ex vivo assay was developed to identify pesticides that can inhibit neuronal ALDH activity. These were investigated for PD associations in a population-based case-control study, the Parkinson's Environment & Genes (PEG) Study. Common variants in the mitochondrial ALDH2 gene were genotyped to assess effect measure modification (statistical interaction) of the pesticide effects by genetic variation. Results: All of the metal-coordinating dithiocarbamates tested (e.g., maneb, ziram), 2 imidazoles (benomyl, triflumizole), 2 dicarboxymides (captan, folpet), and 1 organochlorine (dieldrin) inhibited ALDH activity, potentially via metabolic byproducts (e.g., carbon disulfide, thiophosgene). Fifteen screened pesticides did not inhibit ALDH. Exposures to ALDH-inhibiting pesticides were associated with 2- to 6-fold increases in PD risk; genetic variation in ALDH2 exacerbated PD risk in subjects exposed to ALDH-inhibiting pesticides. Conclusion: ALDH inhibition appears to be an important mechanism through which environmental toxicants contribute to PD pathogenesis, especially in genetically vulnerable individuals, suggesting several potential interventions to reduce PD occurrence or slow or reverse its progression.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0028-3878</s0></fA01><fA02 i1="01"><s0>NEURAI</s0></fA02><fA03 i2="1"><s0>Neurology</s0></fA03><fA05><s2>82</s2></fA05><fA06><s2>5</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Aldehyde dehydrogenase variation enhances effect of pesticides associated with Parkinson disease</s1></fA08><fA11 i1="01" i2="1"><s1>FITZMAURICE (Arthur G.)</s1></fA11><fA11 i1="02" i2="1"><s1>RHODES (Shannon L.)</s1></fA11><fA11 i1="03" i2="1"><s1>COCKBURN (Myles)</s1></fA11><fA11 i1="04" i2="1"><s1>RITZ (Beate)</s1></fA11><fA11 i1="05" i2="1"><s1>BRONSTEIN (Jeff M.)</s1></fA11><fA14 i1="01"><s1>Department of Neurology, David Geffen School of Medicine at UCLA</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Molecular Toxicology, University of California</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="03"><s1>Department of Epidemiology, UCLA Fielding School of Public Health</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ></fA14><fA14 i1="04"><s1>Department of Environmental Health Sciences, UCLA Fielding School of Public Health</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>4 aut.</sZ></fA14><fA14 i1="05"><s1>Department of Preventive Medicine, Keck School of Medicine of USC</s1><s2>Los Angeles</s2><s3>USA</s3><sZ>3 aut.</sZ></fA14><fA14 i1="06"><s1>Parkinson's Disease Research, Education, and Clinical Center, Greater Los Angeles Veterans Affairs Medical Center</s1><s2>Los Angeles</s2><s3>CAN</s3><sZ>5 aut.</sZ></fA14><fA20><s1>419-426</s1></fA20><fA21><s1>2014</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>6345</s2><s5>354000501695730100</s5></fA43><fA44><s0>0000</s0><s1>© 2014 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>40 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>14-0057226</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Neurology</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Objective: The objective of this study was to determine whether environmental and genetic alterations of neuronal aldehyde dehydrogenase (ALDH) enzymes were associated with increased Parkinson disease (PD) risk in an epidemiologic study. Methods: A novel ex vivo assay was developed to identify pesticides that can inhibit neuronal ALDH activity. These were investigated for PD associations in a population-based case-control study, the Parkinson's Environment & Genes (PEG) Study. Common variants in the mitochondrial ALDH2 gene were genotyped to assess effect measure modification (statistical interaction) of the pesticide effects by genetic variation. Results: All of the metal-coordinating dithiocarbamates tested (e.g., maneb, ziram), 2 imidazoles (benomyl, triflumizole), 2 dicarboxymides (captan, folpet), and 1 organochlorine (dieldrin) inhibited ALDH activity, potentially via metabolic byproducts (e.g., carbon disulfide, thiophosgene). Fifteen screened pesticides did not inhibit ALDH. Exposures to ALDH-inhibiting pesticides were associated with 2- to 6-fold increases in PD risk; genetic variation in ALDH2 exacerbated PD risk in subjects exposed to ALDH-inhibiting pesticides. Conclusion: ALDH inhibition appears to be an important mechanism through which environmental toxicants contribute to PD pathogenesis, especially in genetically vulnerable individuals, suggesting several potential interventions to reduce PD occurrence or slow or reverse its progression.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC02 i1="02" i2="X"><s0>002B17A01</s0></fC02><fC02 i1="03" i2="X"><s0>002B17A03</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Maladie de Parkinson</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Aldehyde dehydrogenase (NAD<sup>+</sup>)</s0><s2>FE</s2><s5>09</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Aldehyde dehydrogenase (NAD<sup>+</sup>)</s0><s2>FE</s2><s5>09</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Aldehyde dehydrogenase (NAD<sup>+</sup>)</s0><s2>FE</s2><s5>09</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Pesticide</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Pesticides</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Plaguicida</s0><s5>10</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Oxidoreductases</s0><s2>FE</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Oxidoreductases</s0><s2>FE</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Oxidoreductases</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Enzyme</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0><s2>FE</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0><s5>37</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>37</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>37</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0><s5>38</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>38</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>38</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>39</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>39</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>39</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0><s5>40</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>40</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>40</s5></fC07><fN21><s1>076</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 14-0057226 INIST</NO><ET>Aldehyde dehydrogenase variation enhances effect of pesticides associated with Parkinson disease</ET><AU>FITZMAURICE (Arthur G.); RHODES (Shannon L.); COCKBURN (Myles); RITZ (Beate); BRONSTEIN (Jeff M.)</AU><AF>Department of Neurology, David Geffen School of Medicine at UCLA/Los Angeles/Etats-Unis (1 aut., 4 aut., 5 aut.); Department of Molecular Toxicology, University of California/Los Angeles/Etats-Unis (1 aut., 4 aut., 5 aut.); Department of Epidemiology, UCLA Fielding School of Public Health/Los Angeles/Etats-Unis (2 aut., 4 aut.); Department of Environmental Health Sciences, UCLA Fielding School of Public Health/Los Angeles/Etats-Unis (4 aut.); Department of Preventive Medicine, Keck School of Medicine of USC/Los Angeles/Etats-Unis (3 aut.); Parkinson's Disease Research, Education, and Clinical Center, Greater Los Angeles Veterans Affairs Medical Center/Los Angeles/Canada (5 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Neurology; ISSN 0028-3878; Coden NEURAI; Etats-Unis; Da. 2014; Vol. 82; No. 5; Pp. 419-426; Bibl. 40 ref.</SO><LA>Anglais</LA><EA>Objective: The objective of this study was to determine whether environmental and genetic alterations of neuronal aldehyde dehydrogenase (ALDH) enzymes were associated with increased Parkinson disease (PD) risk in an epidemiologic study. Methods: A novel ex vivo assay was developed to identify pesticides that can inhibit neuronal ALDH activity. These were investigated for PD associations in a population-based case-control study, the Parkinson's Environment & Genes (PEG) Study. Common variants in the mitochondrial ALDH2 gene were genotyped to assess effect measure modification (statistical interaction) of the pesticide effects by genetic variation. Results: All of the metal-coordinating dithiocarbamates tested (e.g., maneb, ziram), 2 imidazoles (benomyl, triflumizole), 2 dicarboxymides (captan, folpet), and 1 organochlorine (dieldrin) inhibited ALDH activity, potentially via metabolic byproducts (e.g., carbon disulfide, thiophosgene). Fifteen screened pesticides did not inhibit ALDH. Exposures to ALDH-inhibiting pesticides were associated with 2- to 6-fold increases in PD risk; genetic variation in ALDH2 exacerbated PD risk in subjects exposed to ALDH-inhibiting pesticides. Conclusion: ALDH inhibition appears to be an important mechanism through which environmental toxicants contribute to PD pathogenesis, especially in genetically vulnerable individuals, suggesting several potential interventions to reduce PD occurrence or slow or reverse its progression.</EA><CC>002B17G; 002B17A01; 002B17A03</CC><FD>Maladie de Parkinson; Pathologie du système nerveux; Aldehyde dehydrogenase (NAD<sup>+</sup>); Pesticide</FD><FG>Oxidoreductases; Enzyme; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central</FG><ED>Parkinson disease; Nervous system diseases; Aldehyde dehydrogenase (NAD<sup>+</sup>); Pesticides</ED><EG>Oxidoreductases; Enzyme; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG><SD>Parkinson enfermedad; Sistema nervioso patología; Aldehyde dehydrogenase (NAD<sup>+</sup>); Plaguicida</SD><LO>INIST-6345.354000501695730100</LO><ID>14-0057226</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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