Brain, Vol. 119, No. 3, 823-830, 1996
© 1996 Guarantors of Brain
research-article |
Alterations in peptide levels in Parkinson's disease and incidental Lewy body disease
1Neurodegeneration Group, Cajal Institute, CSIC Madrid, Spain 2Neurodegenerative Disease Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College London 3University Department of Clinical Neurology, Institute of Neurology, National Hospital for Neurology and Neurosurgery London, UK
Correspondence to:
Correspondence to: Professor P. Jenner, Pharmacology Group, Biomedical Sciences Division, King's College London, Manresa Road, London SW3 6LX, UK
The levels of the neuropeptides Met- and Leu-enkephalin (MET-ENK, LEU-ENK), substance P and neurotensin were measured by a combined high performance liquid chromatography/radioimmunoassay (HPLC/RIA) method in postmortem samples of basal ganglia from Parkinsons disease patients, incidental Lewy body disease patients (presymptomatic Parkinsons disease) and matched controls. Dopamine (DA) levels were reduced in the caudate nucleus and putamen in Parkinsons disease, but unaltered in incidental Lewy body disease. The levels of MET-ENK were reduced in the caudate nucleus, putamen and substantia nigra in Parkinson's disease. Met-enkephalin levels were reduced in the caudate nucleus and in the putamen in incidental Lewy body disease. Leu-enkephalin levels were decreased in the putamen and were undetectable in the substantia nigra in Parkinsons disease. Leu-enkephalin levels were unchanged in incidental Lewy body disease, although there was a tendency to a reduction in putamen. Substance P levels were reduced in the putamen in Parkinsons disease. No significant changes in substance P content were observed in incidental Lewy body disease. Neurotensin levels were increased in the substantia nigra in Parkinsons disease. Neurotensin levels in incidental Lewy body disease were not altered significantly, but tended to parallel the changes in Parkinsons disease. The changes in basal ganglia peptide levels in incidental Lewy body disease generally followed a trend similar to those seen in Parkinsons disease, but were less marked. This suggests that they are an integral part of the pathology of the illness and not secondary to DA neuronal loss or a consequence of prolonged drug therapy.
Parkinson's disease; incidental Lewy body disease; basal ganglia; neuropeptides; high performance liquid chromatography
Received October 3, 1995. Accepted January 30, 1996.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
A. Nilsson, M. Falth, X. Zhang, K. Kultima, K. Skold, P. Svenningsson, and P. E. Andren Striatal Alterations of Secretogranin-1, Somatostatin, Prodynorphin, and Cholecystokinin Peptides in an Experimental Mouse Model of Parkinson Disease Mol. Cell. Proteomics, May 1, 2009; 8(5): 1094 - 1104. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Nadjar, J. M. Brotchie, C. Guigoni, Q. Li, S.-B. Zhou, G.-J. Wang, P. Ravenscroft, F. Georges, A. R. Crossman, and E. Bezard Phenotype of Striatofugal Medium Spiny Neurons in Parkinsonian and Dyskinetic Nonhuman Primates: A Call for a Reappraisal of the Functional Organization of the Basal Ganglia. J. Neurosci., August 23, 2006; 26(34): 8653 - 8661. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. L. Block, G. Li, L. Qin, X. Wu, Z. Pei, T. Wang, B. Wilson, J. Yang, and J. S. Hong Potent regulation of microglia-derived oxidative stress and dopaminergic neuron survival: substance P vs. dynorphin FASEB J, February 1, 2006; 20(2): 251 - 258. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. A. Mooslehner, P. M. Chan, W. Xu, L. Liu, C. Smadja, T. Humby, N. D. Allen, L. S. Wilkinson, and P. C. Emson Mice with Very Low Expression of the Vesicular Monoamine Transporter 2 Gene Survive into Adulthood: Potential Mouse Model for Parkinsonism Mol. Cell. Biol., August 15, 2001; 21(16): 5321 - 5331. [Abstract] [Full Text] [PDF] |
||||



