Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (50)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Kubis, N.
Right arrow Articles by Hirsch, E. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kubis, N.
Right arrow Articles by Hirsch, E. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Brain, Vol. 123, No. 2, 366-373, February 2000
© 2000 Oxford University Press

Preservation of midbrain catecholaminergic neurons in very old human subjects

N. Kubis1, B. A. Faucheux1, G. Ransmayr6, P. Damier1, C. Duyckaerts2, D. Henin3, B. Forette4, Y. Le Charpentier5, J.-J. Hauw2, Y. Agid1 and E. C. Hirsch1

1 INSERM U289 and 2 Laboratoire de Neuropathologie R. Escourolle, INSERM U360, Hôpital de la Salpêtrière, 3 Service d'Anatomo-Pathologie, Hôpital Bichat, 4 Service de Gériatrie, Hôpital Sainte-Périne, 5 Service d'Anatomo-Pathologie, Hôpital de la Pitié, Paris, France and 6 Universität Klinik für Neurologie, Innsbrück, Austria

Correspondence to: E. C. Hirsch, INSERM U289, Hôpital de la Salpêtrière, 47 Blvd de l'Hôpital, 75013, Paris, France

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.

substantia nigra; tyrosine hydroxylase; ageing; human

A8 = peri- and retro-rubral catecholaminergic cell group A8; AChE = acetylcholinesterase; CGS = central grey substance; LC = locus coeruleus; SNpc = substantia nigra pars compacta; TH = tyrosine hydroxylase; VTA = ventral tegmental area


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 NeurologyHome page
J. A. Driver, T. Kurth, J. E. Buring, J. M. Gaziano, and G. Logroscino
Parkinson disease and risk of mortality: A prospective comorbidity-matched cohort study
Neurology, April 15, 2008; 70(16_Part_2): 1423 - 1430.
[Abstract] [Full Text] [PDF]

Home page
 NeurologyHome page
L. Zecca, F. A. Zucca, A. Albertini, E. Rizzio, and R. G. Fariello
A proposed dual role of neuromelanin in the pathogenesis of Parkinson's disease.
Neurology, October 10, 2006; 67(7 Suppl 2): S8 - 11.
[Abstract] [Full Text]

Home page
 Arch NeurolHome page
G. Levy, E. D. Louis, L. Cote, M. Perez, H. Mejia-Santana, H. Andrews, J. Harris, C. Waters, B. Ford, S. Frucht, et al.
Contribution of Aging to the Severity of Different Motor Signs in Parkinson Disease
Arch Neurol, March 1, 2005; 62(3): 467 - 472.
[Abstract] [Full Text] [PDF]

Home page
 Arch NeurolHome page
N. J. Diederich, C. G. Moore, S. E. Leurgans, T. A. Chmura, and C. G. Goetz
Parkinson Disease With Old-Age Onset: A Comparative Study With Subjects With Middle-Age Onset
Arch Neurol, April 1, 2003; 60(4): 529 - 533.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
R. Grondin, W. A. Cass, Z. Zhang, J. A. Stanford, D. M. Gash, and G. A. Gerhardt
Glial Cell Line-Derived Neurotrophic Factor Increases Stimulus-Evoked Dopamine Release and Motor Speed in Aged Rhesus Monkeys
J. Neurosci., March 1, 2003; 23(5): 1974 - 1980.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Pathol.Home page
L Zecca, D Tampellini, M Gerlach, P Riederer, R G Fariello, and D Sulzer
Substantia nigra neuromelanin: structure, synthesis, and molecular behaviour
Mol. Pathol., December 1, 2001; 54(6): 414 - 418.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.