Advertisement

Aspartate, glutamate, and glutamine in platelets of patients with Parkinson’s disease

  • L. H. Rolf
  • Th. Klauke
  • E. W. Fünfgeld
  • G. G. Brune
Conference paper
Part of the Key Topics in Brain Research book series (KEYTOPICS)

Summary

Aspartate, glutamate and glutamine were determined in platelets of 29 patients with Parkinson’s disease (PD) and the results were compared with those of an age matched control group consisting of 24 healthy persons (group A). According to the predominant clinical symptomatology the patients with PD were divided into three groups: group B = patients with tremor (n = 12), group C = patients with akinesia without “on/off” phenomena (n = 11), and group D = patients with akinesia with “on/off” phenomena (n = 6).

Significant decreases of all investigated amino compounds were observed in all groups of patients with PD in comparison with the control group. In addition, aspartate and glutamate were found to be significantly decreased in the group with akinesia and with “on/off” phenomena as compared with the tremor-group. Aspartate was also significantly decreased in patients with akinesia without “on/off” phenomena as compared with the patients with tremor. Glutamine was found to be significantly different between the akinesia groups without and with “on/off” phenomena.

The results point out that platelet aspartate, glutamate and glutamine are significantly decreased in Parkinsonian patients and that there is a correlation between severity of PD and the degree of decreases of the investigated amino compounds.

Keywords

Amyotrophic Lateral Sclerosis Parkinsonian Patient Amino Compound Amino Acid Neurotransmitter High Performance Liquid Chromato 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Berl S, Nicklas WJ (1976) Metabolism of glutamate and related amino acids in brain: effect of drugs that alter catecholamine metabolism. In: Birkmayer W, Hornykiewicz O (eds) Advances in parkinsonism. Editiones Roche, Basel, pp 193–204Google Scholar
  2. Fagg CE, Foster AC (1983) Amino acid neurotransmitters and their pathways in the mammalian central nervous system. Neuroscience 9: 701–719PubMedCrossRefGoogle Scholar
  3. Gordon JL, Milner AJ (1976) Blood platelets as multifunctional cells. In: Gordon JL (ed) Platelets in biology and pathology. North-Holland, Amsterdam, pp 11–21Google Scholar
  4. Hassler R (1966) Thalamus regulation of muscle tone and the speed of movements. In: Purpura DP, Yahr MD (eds) The thalamus. Columbia University Press, New York, pp 418–438Google Scholar
  5. Hassler R, Nitsch C, Lee HL (1980) The role of eight putative transmitters in the nine types of synapses in rat caudate-putamen. In: Rinne UK, Klingler M, Stamm G (eds) Parkinson’s disease—current progress, problems and management. Elsevier/North-Holland Biomedical Press, Amsterdam, pp 61–91Google Scholar
  6. Lenda K, Svenneby G (1981) Rapid high performance liquid chromatographic determination of amino acids in synaptosomal extracts. J Chromatogr 198: 516–519CrossRefGoogle Scholar
  7. Lloyd KG, Möhler H, Hertz P, Bartholini G (1975) Distribution of choline acetyltransferase and glutamic acid decarboxylase within the substantia nigra and other brain regions from control and parkinsonian patients. J Neurochem 25: 785–789CrossRefGoogle Scholar
  8. Ludolph AC, Rolf LH (1988) Unpublished observationsGoogle Scholar
  9. Mangano RM, Schwarzc (1981) The human platelets as a model for the glutaminergic neuron. Platelet uptake of L-glutamate. J Neurochem 36: 1067–1076PubMedCrossRefGoogle Scholar
  10. Manyam BV, Ferraro TN, Hare TA (1988) Cerebrospinal fluid amino compounds in Parkinson’s disease. Arch Neurol 45: 48–51PubMedCrossRefGoogle Scholar
  11. McGeer EG, Staines WA, McGeer PL (1984) Neurotransmitters in the basal ganglia. Can J Neurol Sci 11: 89–99PubMedGoogle Scholar
  12. Olney JW, Ho OL, Rhee V (1971) Cytotoxic effects of acidic and sulphur containing amino acids on the infant mouse central nervous system. Exper Brain Res 14: 61–76Google Scholar
  13. Perry TL, Hansen S, Jones K (1987) Brain glutamate deficiency in amyotrophic lateral sclerosis. Neurology 37: 1845–1848PubMedGoogle Scholar
  14. Riederer P, Jellinger K (1983) Morphologie und Pathobiochemie der Parkinson-Krankheit In: Gänshirt (Hrsg) Pathophysiologie, Klinik und Therapie des Parkinsonismus. Editiones Roche, Basel, S 31–50Google Scholar
  15. Rogers J, Morrison JH (1985) Quantitative morphology and regional laminar distributions of senile plaques in Alzheimer’s disease. J Neurosci 5: 2801–2808PubMedGoogle Scholar
  16. Rolf LH, Schlake HP, Brune GG (1983) Plasmafaktoren und Migräne. In: Soyka D (Hrsg) Migräne: Pathogenese–Pharmakologie–Therapie. Enke, Stuttgart, S 79–97Google Scholar
  17. Spencer PS, Nunn PB, Hugon J, Ludolph A, Roy DN (1986) Motor neurone disease on Guam: possible role of a food neurotoxin. Lancet 1: 965PubMedCrossRefGoogle Scholar
  18. Spencer PS, Hugon J, Ludolph A, Nunn PB, Ross SM, Roy DN, Schaumburg HH (1987) Discovery and partial characterization of primate motor-system toxins. In: Ciba Foundation Symposium 126; Selective neuronal death. Wiley, Chichester, pp 221–237Google Scholar

Copyright information

© Springer-Verlag/Wien 1989

Authors and Affiliations

  • L. H. Rolf
    • 1
  • Th. Klauke
    • 1
  • E. W. Fünfgeld
    • 2
  • G. G. Brune
    • 1
  1. 1.Klinik und Poliklinik für NeurologieWestfälischen Wilhelms-UniversitätMünsterFederal Republic of Germany
  2. 2.Schloßklinik WittgensteinBad LaaspheFederal Republic of Germany

Personalised recommendations