Hostname: page-component-78c5997874-dh8gc Total loading time: 0 Render date: 2024-11-03T00:34:31.790Z Has data issue: false hasContentIssue false

Cerebrospinal Fluid pH and Monoamine and Glucolytic Metabolites in Alzheimer's Disease

Published online by Cambridge University Press:  29 January 2018

C. G. Gottfries
Affiliation:
Department of Psychiatry, University Hospital, Umea, Sweden
Åke Kjällquist
Affiliation:
Department of Neurosurgery, University Hospital, Lund, Sweden
Urban Pontén
Affiliation:
Department of Neurosurgery, University Hospital, Lund, Sweden
B. E. Roos
Affiliation:
Department of Pharmacology, University of Göteborg, Sweden
G. Sundbärg
Affiliation:
Department of Neurosurgery, University Hospital, Lund, Sweden

Extract

Determinations of acid monoamine metabolites, such as homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA), in cerebrospinal fluid (CSF) give valid information on the metabolism of the corresponding amines in the brain tissue (Moir et al., 1970; Roos, 1970). The monoamine metabolites in the CSF are related to age. The concentrations of HVA and 5-HIAA increase with age (Gottfries et al., 1971). Probenecid blocks the elimination of HVA and 5-HIAA from brain tissue to blood (Neff et al., 1964, 1967; Werdinius, 1966) and from CSF to blood (Guldberg et al., 1966; Olsson and Roos, 1968). Probenecid thus normally induces an increase in the concentrations of the acid monoamine metabolites in the CSF, which is related to the turnover of monoamines in the brain tissue.

Type
Research Article
Copyright
Copyright © Royal College of Psychiatrists, 1974 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Andén, N. E., Roos, B. E., and Werdinius, B. (1963). ‘On the occurrence of homovanillic acid in brain and cerebrospinal fluid and its determination by a fluorometric method.’ Life Science, 7, 448–58.Google Scholar
Ashcroft, G. W., and Sharman, D. F. (1960), ‘5-hydroxyindoles in human cerebrospinal fluids.’ Nature, 186, 1050.CrossRefGoogle ScholarPubMed
Blessed, G., and Tomlinsen, B. E. (1965). ‘Senile plaques and intellectual deterioration in old age’, in Psychiatric Disorders in the Aged, pp. 310–21. Report on the Symposium held by the World Psychiatric Association in London. Manchester: Geigy.Google Scholar
Cohen, P. J., Alexander, S. C., Smith, T. C., Reivich, M., and Wollman, H. (1967). ‘Effects of hypoxia and normocarbia on cerebral blood flow and metabolism in conscious man.’ Journal of Applied Physiology, 23, 183–9.CrossRefGoogle ScholarPubMed
Gottfries, C. G., and Gottfries, I. (1968). Geriatriskt Skattningsschema. III. Stencil. Lunds Universitet.Google Scholar
Gottfries, C. G., Gottfries, I. and Roos, B. E. (1969). ‘Homovanillic acid and 5-hydroxyindoleacetic acid in the cerebrospinal fluid of patients with senile dementia, presenile dementia and parkinsonism.’ Journal of Neurochemistry, 16, 1341–5.CrossRefGoogle ScholarPubMed
Gottfries, C. G., Gottfries, I. and Roos, B. E. (1970). ‘Homovanillic acid and 5-hydroxyindoleacetic acid in cerebrospinal fluid related to rated mental and motor impairment in senile and presenile dementia.’ Acta Psychiatrica Scandinavica, 46, 99105.Google ScholarPubMed
Gottfries, C. G., Gottfries, I. Johansson, B., Olsson, R., Persson, T., Roos, B. E., and Sjöström, R. (1971). ‘Acid monoamine metabolites in human cerebrospinal fluid and their relations to age and sex.’ Neuropharmacology, 10, 665–72. London: Pergamon Press.Google Scholar
Granholm, L., and Siesjö, B. K. (1971). Signs of Tissue Hypoxia in Infantile Hydrocephalus . Supplement 22. Hydrocephalus and Spina Bifida, pp. 73–7.Google Scholar
Granholm, L., and Kåostrôm, , E. To be published.Google Scholar
Guldberg, H. C., Ashcroft, G. W., and Crawford, T. B. B. (1966). ‘Concentrations of 5-hydroxyindoleacetic acid and homovanillic acid in the cerebrospinal fluid of the dog before and during treatment with probenecid.’ Life Science, 5, 1571–5.Google ScholarPubMed
Hohorst, H. J., Kreutz, F. H., and Bücher, T. (1959). ‘Über Metabolitgehalte und Metabolit-Konzentrationen in der Leber der Ratte.’ Biochemische Zeitschrift, 332, 18.Google Scholar
Ingvar, D. H., and Gustafson, L. (1970). ‘Regional cerebral blood flow in organic dementia with early onset.’ Acta Neurologica Scandinavica, Supplement 43, Volume 46.Google Scholar
Kaasik, A. E., Nilsson, L., and Siesjö, B. K. (1970). ‘The effect of asphyxia upon lactate, pyruvate and bicarbonate concentrations of brain tissue and coesternal CSF, and upon the tissue concentrations of phosphocreatine and adenine nucleotides in anesthetized rats.’ Acta Physiologica Scandinavica, 78, 433.CrossRefGoogle ScholarPubMed
Kjällqubt, Å., Pontén, U., and Sundbärg, G. (1973). Unpublished results.Google Scholar
Kullberg, G., Pontén, U., and Sundbärg, , G. To be published.Google Scholar
Lassen, N. A., Munch, O., and Tottey, E. R. (1957). ‘Mental function and cerebral oxygen consumption in organic dementia.’ Archives of Neurology and Psychiatry (Chic.), 77, 126.CrossRefGoogle ScholarPubMed
Mitchell, R. A., Herbert, D. A., and Carman, C. T. (1965). ‘Acid-base constants and temperature coefficients for cerebrospinal fluid.’ Journal of Applied Physiology, 20, 2730.Google Scholar
Mom, A. T. B., Ashcroft, G. W., Crawford, T. B. B., Eccleston, D., and Guldberg, H. C. (1970). ‘Cerebral metabolites in cerebrospinal fluid as a biochemical approach to the brain.’ Brain, 93, 357–68.Google Scholar
Neff, N. H., Tozer, T. N., and Brodie, B. B. (1964). ‘A specialized transport system to transfer 5-HIAA directly from brain to blood.’ Pharmacologist, 6, 162.Google Scholar
Neff, N. H., Tozer, T. N., and Brodie, B. B. (1967). ‘Application of steady-state kinetics to studies of the transfer of 5-hydroxyindoleacetic acid from brain to plasma.’ Journal of Pharmacology and Experiments Therapeutics, 158, 214–18.Google Scholar
Obrist, W. D., Chivian, E., Cronqvist, S., and Ingvar, D. H. (1970). ‘Regional cerebral blood flow in senile and presenile dementia.’ Neurology, 20, 4, 315–22.CrossRefGoogle ScholarPubMed
Olsson, R., and Roos, B. E. (1968). ‘Concentration of 5-hydroxyindoleacetic acid and homovanillic acid in the cerebrospinal fluid after treatment with probenecid in patients with Parkinson's disease.’ Nature, 219, 502–3.CrossRefGoogle ScholarPubMed
Pontén, U., Kjällquiest, Å., SiESJö, B. K., sundbärg, G., and Svendgaard, N. (1968). ‘Relation of selective acidosis of CSF to increased lactate/pyruvate ratios.’ Scandinavian Journal of Clinical and Laboratory Investigation. Suppl. 102, IX:D.Google Scholar
Posner, J. B., Swanson, A. G., and Plum, F. (1965). ‘Acid-base balance in cerebrospinal fluid.’ Archives of Neurology, 12, 479–96.CrossRefGoogle ScholarPubMed
Roos, B. E., and Sjöström, R. (1969). ‘5-hydroxyindoleacetic acid (and homovanillic acid) levels in the cerebrospinal fluid after probenecid application in patient with manic depressive psychosis.’ Pharmacologica Clinica, 1, 153–5.Google Scholar
Roos, B. E., (1970). ‘Metabolites of the monoamines in the cerebrospinal fluid’, in Monoamines et noyaux gris centraux. Symposium Bel-Air IV, Geneve.Google Scholar
Scheinberg, P. (1950). ‘Cerebral blood flow in vascular disease of the brain.’ American Journal of Medicine, 8, 139.CrossRefGoogle ScholarPubMed
Siesjö, B. K., and Nilsson, L. (1971). ‘The influence of arterial hypoxemia upon labile phosphates and upon extracellular and intracellular lactate and pyruvate concentration in the rat brain.’ Scandinavian Journal of Clinical and Laboratory Investigation, 27, 8396.Google Scholar
Sjögren, H., and Sourrander, P. (1961). ‘Histopathological studies in Alzheimer's disease.’ IV Intern. Kongr. für Neur-pathologie, III, iv, 319–24.Google Scholar
Sjögren, T., Sjögren, H., and Lindgren, Å. G. H. (1952). ‘Morbus Alzheimer and Morbus Pick. A genetic, clinical and patho-anatomical study.’ Acta psychiat. neurol. scand. Suppl. 82.Google Scholar
Svenningsen, N. W., and Siesjö, B. K. (1972). ‘Cerebrospinal fluid lactate/pyruvate ratio in normal and asphyxiated neonates.’ Acta Psychiatrica Scandinavica, 61, 117–24.Google ScholarPubMed
Werdinius, B. (1966). ‘Effect of probenecid on the level of homovanillic acid in the corpus striatum.’ Journal of Pharmacology, 18, 546–7.Google ScholarPubMed
Submit a response

eLetters

No eLetters have been published for this article.