Preservation of midbrain catecholaminergic neurons in very old human subjects
Identifieur interne : 001088 ( Istex/Checkpoint ); précédent : 001087; suivant : 001089Preservation of midbrain catecholaminergic neurons in very old human subjects
Auteurs : N. Kubis ; B. A. Faucheux ; G. Ransmayr [Autriche] ; P. Damier ; C. Duyckaerts ; D. Henin ; B. Forette ; Y. Le Charpentier [France] ; J.-J. Hauw ; Yves Agid [France] ; E. C. HirschSource :
- Brain [ 0006-8950 ] ; 2000-02.
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- KwdEn :
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, peri- and 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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DOI: 10.1093/brain/123.2.366
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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><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><noCountry><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. 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Ransmayr</name></noRegion></country><country name="France"><region name="Île-de-France"><name sortKey="Le Charpentier, Y" sort="Le Charpentier, Y" uniqKey="Le Charpentier Y" first="Y." last="Le Charpentier">Y. Le Charpentier</name></region><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y." last="Agid">Yves Agid</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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