Preservation of midbrain catecholaminergic neurons in very old human subjects
Identifieur interne : 001185 ( PascalFrancis/Checkpoint ); précédent : 001184; suivant : 001186Preservation of midbrain catecholaminergic neurons in very old human subjects
Auteurs : N. Kubis [France] ; B. A. Faucheux [France] ; G. Ransmayr [Autriche] ; P. Damier [France] ; C. Duyckaerts [France] ; D. Henin [France] ; B. Forette [France] ; Y. Le Charpentier [France] ; J.-J. Hauw [France] ; Yves Agid [France] ; E. C. Hirsch [France]Source :
- Brain [ 0006-8950 ] ; 2000.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Analyse quantitative, Adulte, Personne âgée.
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Abstract
Parkinson's disease is characterized by a progressive degeneration of dopaminergic neurons in the midbrain, yet the cause of this neuronal loss is still unknown. It has been hypothesized that Parkinson's disease could be the consequence of accelerated ageing. In order to reveal a possible common process during ageing and Parkinson's disease neurodegeneration, catecholaminergic neurons of five anatomical regions of the brainstem (substantia nigra, central grey substance, ventral tegmental area, periand retrorubral area, and locus coeruleus) have been quantified using immunohistochemical staining for tyrosine hydroxylase (TH) on regularly spaced sections, between the rostral and caudal poles of the mesencephalon and in the rostral pole of the pons, in post-mortem samples of 21 control subjects who died at ages 44-110 years. No statistically significant loss of TH positive neurons was observed in the older subjects, either in the substantia nigra or in the other midbrain regions that are known to degenerate to a lesser degree in Parkinson's disease. Furthermore, in the later regions no neuronal loss was observed from age 44 to 80 years, indicating that this result is not dependent on the inclusion of 'supernormal' very old people. These results suggest that from age 44 to 110 years, ageing in control adults is not, or is scarcely, accompanied by catecholaminergic cell loss in the midbrain and hence Parkinson's disease is probably not caused by an acceleration of a degenerative process during ageing.
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Escourolle, INSERM U360, Hôpital de la Salpêtrière</wicri:noRegion></affiliation></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y." last="Agid">Yves Agid</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM U289, Hôpital de la Salpêtrière</s1><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Hôpital de la Salpêtrière</wicri:noRegion><wicri:noRegion>INSERM U289, Hôpital de la Salpêtrière</wicri:noRegion><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName></affiliation></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E. C." last="Hirsch">E. C. 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Kubis</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM U289, Hôpital de la Salpêtrière</s1><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Hôpital de la Salpêtrière</wicri:noRegion><wicri:noRegion>INSERM U289, Hôpital de la Salpêtrière</wicri:noRegion></affiliation></author><author><name sortKey="Faucheux, B A" sort="Faucheux, B A" uniqKey="Faucheux B" first="B. A." last="Faucheux">B. A. Faucheux</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM U289, Hôpital de la Salpêtrière</s1><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Hôpital de la Salpêtrière</wicri:noRegion><wicri:noRegion>INSERM U289, Hôpital de la Salpêtrière</wicri:noRegion></affiliation></author><author><name sortKey="Ransmayr, G" sort="Ransmayr, G" uniqKey="Ransmayr G" first="G." last="Ransmayr">G. Ransmayr</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Universität Klinik für Neurologie</s1><s2>Innsbrück</s2><s3>AUT</s3><sZ>3 aut.</sZ></inist:fA14><country>Autriche</country><wicri:noRegion>Universität Klinik für Neurologie</wicri:noRegion></affiliation></author><author><name sortKey="Damier, P" sort="Damier, P" uniqKey="Damier P" first="P." last="Damier">P. Damier</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM U289, Hôpital de la Salpêtrière</s1><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Hôpital de la Salpêtrière</wicri:noRegion><wicri:noRegion>INSERM U289, Hôpital de la Salpêtrière</wicri:noRegion></affiliation></author><author><name sortKey="Duyckaerts, C" sort="Duyckaerts, C" uniqKey="Duyckaerts C" first="C." last="Duyckaerts">C. Duyckaerts</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Laboratoire de Neuropathologie R. Escourolle, INSERM U360, Hôpital de la Salpêtrière</s1><s3>FRA</s3><sZ>5 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Hôpital de la Salpêtrière</wicri:noRegion><wicri:noRegion>Laboratoire de Neuropathologie R. Escourolle, INSERM U360, Hôpital de la Salpêtrière</wicri:noRegion></affiliation></author><author><name sortKey="Henin, D" sort="Henin, D" uniqKey="Henin D" first="D." last="Henin">D. Henin</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Service d'Anatomo-Pathologie, Hôpital Bichat</s1><s3>FRA</s3><sZ>6 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Hôpital Bichat</wicri:noRegion><wicri:noRegion>Service d'Anatomo-Pathologie, Hôpital Bichat</wicri:noRegion></affiliation></author><author><name sortKey="Forette, B" sort="Forette, B" uniqKey="Forette B" first="B." last="Forette">B. Forette</name><affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Service de Gériatrie, Hôpital Sainte-Périne</s1><s3>FRA</s3><sZ>7 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Hôpital Sainte-Périne</wicri:noRegion><wicri:noRegion>Service de Gériatrie, Hôpital Sainte-Périne</wicri:noRegion></affiliation></author><author><name sortKey="Le Charpentier, Y" sort="Le Charpentier, Y" uniqKey="Le Charpentier Y" first="Y." last="Le Charpentier">Y. Le Charpentier</name><affiliation wicri:level="3"><inist:fA14 i1="06"><s1>Service d'Anatomo-Pathologie, Hôpital de la Pitié</s1><s2>Paris</s2><s3>FRA</s3><sZ>8 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Hauw, J J" sort="Hauw, J J" uniqKey="Hauw J" first="J.-J." last="Hauw">J.-J. Hauw</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Laboratoire de Neuropathologie R. Escourolle, INSERM U360, Hôpital de la Salpêtrière</s1><s3>FRA</s3><sZ>5 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Hôpital de la Salpêtrière</wicri:noRegion><wicri:noRegion>Laboratoire de Neuropathologie R. Escourolle, INSERM U360, Hôpital de la Salpêtrière</wicri:noRegion></affiliation></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y." last="Agid">Yves Agid</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM U289, Hôpital de la Salpêtrière</s1><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Hôpital de la Salpêtrière</wicri:noRegion><wicri:noRegion>INSERM U289, Hôpital de la Salpêtrière</wicri:noRegion><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName></affiliation></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E. C." last="Hirsch">E. C. Hirsch</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM U289, Hôpital de la Salpêtrière</s1><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>France</country><wicri:noRegion>Hôpital de la Salpêtrière</wicri:noRegion><wicri:noRegion>INSERM U289, Hôpital de la Salpêtrière</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Brain</title><title level="j" type="abbreviated">Brain</title><idno type="ISSN">0006-8950</idno><imprint><date when="2000">2000</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Brain</title><title level="j" type="abbreviated">Brain</title><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Age</term><term>Brain stem</term><term>Catecholaminergic neuron</term><term>Elderly</term><term>Evolution</term><term>Immunohistochemistry</term><term>Physiology</term><term>Quantitative analysis</term><term>Senescence</term><term>Tyrosine 3-monooxygenase</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Sénescence</term><term>Age</term><term>Neurone catécholaminergique</term><term>Analyse quantitative</term><term>Tronc cérébral</term><term>Immunohistochimie</term><term>Tyrosine 3-monooxygenase</term><term>Physiologie</term><term>Evolution</term><term>Adulte</term><term>Personne âgée</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Analyse quantitative</term><term>Adulte</term><term>Personne âgée</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease is characterized by a progressive degeneration of dopaminergic neurons in the midbrain, yet the cause of this neuronal loss is still unknown. It has been hypothesized that Parkinson's disease could be the consequence of accelerated ageing. In order to reveal a possible common process during ageing and Parkinson's disease neurodegeneration, catecholaminergic neurons of five anatomical regions of the brainstem (substantia nigra, central grey substance, ventral tegmental area, periand retrorubral area, and locus coeruleus) have been quantified using immunohistochemical staining for tyrosine hydroxylase (TH) on regularly spaced sections, between the rostral and caudal poles of the mesencephalon and in the rostral pole of the pons, in post-mortem samples of 21 control subjects who died at ages 44-110 years. No statistically significant loss of TH positive neurons was observed in the older subjects, either in the substantia nigra or in the other midbrain regions that are known to degenerate to a lesser degree in Parkinson's disease. Furthermore, in the later regions no neuronal loss was observed from age 44 to 80 years, indicating that this result is not dependent on the inclusion of 'supernormal' very old people. These results suggest that from age 44 to 110 years, ageing in control adults is not, or is scarcely, accompanied by catecholaminergic cell loss in the midbrain and hence Parkinson's disease is probably not caused by an acceleration of a degenerative process during ageing.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0006-8950</s0></fA01><fA03 i2="1"><s0>Brain</s0></fA03><fA05><s2>123</s2></fA05><fA06><s3>p.2</s3></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Preservation of midbrain catecholaminergic neurons in very old human subjects</s1></fA08><fA11 i1="01" i2="1"><s1>KUBIS (N.)</s1></fA11><fA11 i1="02" i2="1"><s1>FAUCHEUX (B. A.)</s1></fA11><fA11 i1="03" i2="1"><s1>RANSMAYR (G.)</s1></fA11><fA11 i1="04" i2="1"><s1>DAMIER (P.)</s1></fA11><fA11 i1="05" i2="1"><s1>DUYCKAERTS (C.)</s1></fA11><fA11 i1="06" i2="1"><s1>HENIN (D.)</s1></fA11><fA11 i1="07" i2="1"><s1>FORETTE (B.)</s1></fA11><fA11 i1="08" i2="1"><s1>LE CHARPENTIER (Y.)</s1></fA11><fA11 i1="09" i2="1"><s1>HAUW (J.-J.)</s1></fA11><fA11 i1="10" i2="1"><s1>AGID (Y.)</s1></fA11><fA11 i1="11" i2="1"><s1>HIRSCH (E. C.)</s1></fA11><fA14 i1="01"><s1>INSERM U289, Hôpital de la Salpêtrière</s1><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ></fA14><fA14 i1="02"><s1>Universität Klinik für Neurologie</s1><s2>Innsbrück</s2><s3>AUT</s3><sZ>3 aut.</sZ></fA14><fA14 i1="03"><s1>Laboratoire de Neuropathologie R. Escourolle, INSERM U360, Hôpital de la Salpêtrière</s1><s3>FRA</s3><sZ>5 aut.</sZ><sZ>9 aut.</sZ></fA14><fA14 i1="04"><s1>Service d'Anatomo-Pathologie, Hôpital Bichat</s1><s3>FRA</s3><sZ>6 aut.</sZ></fA14><fA14 i1="05"><s1>Service de Gériatrie, Hôpital Sainte-Périne</s1><s3>FRA</s3><sZ>7 aut.</sZ></fA14><fA14 i1="06"><s1>Service d'Anatomo-Pathologie, Hôpital de la Pitié</s1><s2>Paris</s2><s3>FRA</s3><sZ>8 aut.</sZ></fA14><fA20><s1>366-373</s1></fA20><fA21><s1>2000</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>998</s2><s5>354000081821320140</s5></fA43><fA44><s0>0000</s0><s1>© 2000 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>34 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>00-0094542</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Brain</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>Parkinson's disease is characterized by a progressive degeneration of dopaminergic neurons in the midbrain, yet the cause of this neuronal loss is still unknown. It has been hypothesized that Parkinson's disease could be the consequence of accelerated ageing. In order to reveal a possible common process during ageing and Parkinson's disease neurodegeneration, catecholaminergic neurons of five anatomical regions of the brainstem (substantia nigra, central grey substance, ventral tegmental area, periand retrorubral area, and locus coeruleus) have been quantified using immunohistochemical staining for tyrosine hydroxylase (TH) on regularly spaced sections, between the rostral and caudal poles of the mesencephalon and in the rostral pole of the pons, in post-mortem samples of 21 control subjects who died at ages 44-110 years. No statistically significant loss of TH positive neurons was observed in the older subjects, either in the substantia nigra or in the other midbrain regions that are known to degenerate to a lesser degree in Parkinson's disease. Furthermore, in the later regions no neuronal loss was observed from age 44 to 80 years, indicating that this result is not dependent on the inclusion of 'supernormal' very old people. These results suggest that from age 44 to 110 years, ageing in control adults is not, or is scarcely, accompanied by catecholaminergic cell loss in the midbrain and hence Parkinson's disease is probably not caused by an acceleration of a degenerative process during ageing.</s0></fC01><fC02 i1="01" i2="X"><s0>002A25L</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Sénescence</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Senescence</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Senescencia</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Age</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Age</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Edad</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Neurone catécholaminergique</s0><s5>04</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Catecholaminergic neuron</s0><s5>04</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Neurona catecolaminérgica</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Analyse quantitative</s0><s5>05</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Quantitative analysis</s0><s5>05</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Análisis cuantitativo</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Tronc cérébral</s0><s5>07</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Brain stem</s0><s5>07</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Tronco cerebral</s0><s5>07</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Immunohistochimie</s0><s5>10</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Immunohistochemistry</s0><s5>10</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Inmunohistoquímica</s0><s5>10</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Tyrosine 3-monooxygenase</s0><s2>FE</s2><s5>11</s5><s6>Tyrosine «3»-monooxygenase</s6></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Tyrosine 3-monooxygenase</s0><s2>FE</s2><s5>11</s5><s6>Tyrosine «3»-monooxygenase</s6></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Tyrosine 3-monooxygenase</s0><s2>FE</s2><s5>11</s5><s6>Tyrosine «3»-monooxygenase</s6></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Physiologie</s0><s5>17</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Physiology</s0><s5>17</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Fisiología</s0><s5>17</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Evolution</s0><s5>18</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Evolution</s0><s5>18</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Evolución</s0><s5>18</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Adulte</s0><s5>20</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Adult</s0><s5>20</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Adulto</s0><s5>20</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Personne âgée</s0><s5>21</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Elderly</s0><s5>21</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Anciano</s0><s5>21</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></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Homme</s0></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Human</s0></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Hombre</s0></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Encéphale</s0><s5>53</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Brain (vertebrata)</s0><s5>53</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Encéfalo</s0><s5>53</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>54</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system</s0><s5>54</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>54</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Anatomopathologie</s0><s5>61</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Pathology</s0><s5>61</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Anatomía patológica</s0><s5>61</s5></fC07><fN21><s1>066</s1></fN21></pA></standard></inist><affiliations><list><country><li>Autriche</li><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li></settlement><orgName><li>Hôpital de la Salpêtrière</li></orgName></list><tree><country name="France"><noRegion><name sortKey="Kubis, N" sort="Kubis, N" uniqKey="Kubis N" first="N." last="Kubis">N. Kubis</name></noRegion><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y." last="Agid">Yves Agid</name><name sortKey="Damier, P" sort="Damier, P" uniqKey="Damier P" first="P." last="Damier">P. Damier</name><name sortKey="Duyckaerts, C" sort="Duyckaerts, C" uniqKey="Duyckaerts C" first="C." last="Duyckaerts">C. Duyckaerts</name><name sortKey="Faucheux, B A" sort="Faucheux, B A" uniqKey="Faucheux B" first="B. A." last="Faucheux">B. A. Faucheux</name><name sortKey="Forette, B" sort="Forette, B" uniqKey="Forette B" first="B." last="Forette">B. Forette</name><name sortKey="Hauw, J J" sort="Hauw, J J" uniqKey="Hauw J" first="J.-J." last="Hauw">J.-J. Hauw</name><name sortKey="Henin, D" sort="Henin, D" uniqKey="Henin D" first="D." last="Henin">D. Henin</name><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E. C." last="Hirsch">E. C. Hirsch</name><name sortKey="Le Charpentier, Y" sort="Le Charpentier, Y" uniqKey="Le Charpentier Y" first="Y." last="Le Charpentier">Y. Le Charpentier</name></country><country name="Autriche"><noRegion><name sortKey="Ransmayr, G" sort="Ransmayr, G" uniqKey="Ransmayr G" first="G." last="Ransmayr">G. Ransmayr</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Preservation of midbrain catecholaminergic neurons in very old human subjects
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