Time course of nigrostriatal degeneration in parkinson's disease

It could be shown that the post mortem analysis of biogenic amines, precursors, and metabolites in the human brain are influenced by various parameters. 1. The patient's medical history; long term observation of the course of the disease; age; sex. 2. Terminal illness; duration of terminal illness. 3. Previous treatment with drugs; last drugs. 4. Time interval between last drug treatment and death; time of day and date of last drug consumption. 5. Rapidity of death; time of death; duration of coma. 6. Changes occurring in tissues before death; patient's constitution during terminal illness. 7. Changes in concentration of the biogenic amines, precursors, and metabolites depending on the patient's age. 8. Time between death and necropsy. 9. Dissection of specimen. 10. Period of storage; temperature of storage. 11. Chronobiological rhythm of substances. 12. Methods of assay. 13. Homogeneity of all mentioned parameters in the control group and patient group. The patient's medical history; long term observation of the course of the disease; age; sex. Terminal illness; duration of terminal illness. Previous treatment with drugs; last drugs. Time interval between last drug treatment and death; time of day and date of last drug consumption. Rapidity of death; time of death; duration of coma. Changes occurring in tissues before death; patient's constitution during terminal illness. Changes in concentration of the biogenic amines, precursors, and metabolites depending on the patient's age. Time between death and necropsy. Dissection of specimen. Period of storage; temperature of storage. Chronobiological rhythm of substances. Methods of assay. Homogeneity of all mentioned parameters in the control group and patient group. For the first time it could be demonstrated that the time course of nigrostriatal degeneration, independent of the age of the parkinsonian at the beginning of the illness, is linear for the last stage and the denervation progressively increases as the duration of illness progresses.

[1]  O. Hornykiewicz,et al.  Der L-Dioxyphenylalanin (=L-DOPA)-Effekt beim Parkinson-Syndrom des Menschen: Zur Pathogenese und Behandlung der Parkinson-Akinese , 2004, Archiv für Psychiatrie und Nervenkrankheiten.

[2]  H. Weissbach,et al.  THE DISTRIBUTION OF SEROTONIN, 5‐HYDROXYTRYPTOPHAN DECARBOXYLASE, AND MONOAMINE OXIDASE IN BRAIN * , 1957, Journal of neurochemistry.

[3]  E. Neumayer,et al.  Die moderne medikamentöse Behandlung des Parkinsonismus , 1972, Zeitschrift für Neurologie.

[4]  D. Robinson.  Changes in monoamine oxidase and monoamines with human development and aging. , 1975, Federation proceedings.

[5]  T. Nagatsu,et al.  A 24-hour rhythm in human serum dopamine-β-hydroxylase activity , 1974, Experientia.

[6]  T. Chase,et al.  L-Dopa-Induced Release of Cerebral Monoamines , 1970, Science.

[7]  W. B. Quay.  Differential extractions for the spectrophotofluorometric measurement of diverse 5-hydroxy- and 5-methoxyindoles. , 1963, Analytical biochemistry.

[8]  Samuil Michailovič Blinkov,et al.  Das Zentralnervensystem in Zahlen und Tabellen , 1968 .

[9]  R. Wurtman,et al.  Control of brain serotonin by the diet. , 1974, Advances in neurology.

[10]  G. Biggio,et al.  Daily changes of free serum tryptophan in humans. , 1974, Life sciences.

[11]  O. Hornykiewicz,et al.  Serotonin and 5-hydroxyindoleacetic acid in discrete areas of the brainstem of suicide victims and control patients. , 1974, Advances in biochemical psychopharmacology.

[12]  A. Carandente.  Chronobiological aspects of endocrinology. , 1974, Chronobiologia.

[13]  A. Anton,et al.  THE DISTRIBUTION OF DOPAMINE AND DOPA IN VARIOUS ANIMALS AND A METHOD FOR THEIR DETERMINATION IN DIVERSE BIOLOGICAL MATERIAL. , 1964, The Journal of pharmacology and experimental therapeutics.

[14]  E. Rosengren,et al.  Effect of iproniazid on monoamines and monoamine oxidase in human brain , 1962, Experientia.

[15]  B. Winblad,et al.  LOWERED MONOAMINE OXIDASE ACTIVITY IN BRAINS FROM ALCOHOLIC SUICIDES , 1975, Journal of neurochemistry.

[16]  R. Yamazaki,et al.  Circadian fluctuation of brain acetylcholine in rats. I. On the variations in the total brain and discrete brain areas. , 1975, Life sciences.

[17]  J. Dominic.  SUPPRESSION OF BRAIN SEROTONIN SYNTHESIS AND METABOLISM BY BENZODIAZEPINE MINOR TRANQUILIZERS , 1973 .

[18]  A. Carlsson.  The "on-off" effect. , 1974, Advances in neurology.

[19]  W. Rick,et al.  Optimierung der Diagnostik , 1973 .

[20]  G. Ashcroft,et al.  Drug-induced changes in the concentration of 5-OR indolyl compounds in cerebrospinal fluid and caudate nucleus. , 1962, British journal of pharmacology and chemotherapy.

[21]  A. Pletscher,et al.  Decrease of cerebral 5‐hydroxytryptamine by 3,4‐dihydroxyphenylalanine after inhibition of extracerebral decarboxylase , 1968, The Journal of pharmacy and pharmacology.

[22]  T. Perry,et al.  REGIONAL DISTRIBUTION OF AMINO ACIDS IN HUMAN BRAIN OBTAINED AT AUTOPSY , 1971, Journal of neurochemistry.

[23]  W. J. Nicholson,et al.  EFFECT OF MONOAMINE-OXIDASE INHIBITORS ON THE CONCENTRATIONS OF 5-HYDROXYTRYPTAMINE IN THE HUMAN BRAIN. , 1965, Lancet.

[24]  W. Burkard,et al.  DECREASE OF CEREBRAL 5-HYDROXYTRYPTAMINE AND 5-HYDROXYINDOLACETIC ACID BY AN ARYLALKYLAMINE. , 1963, Life sciences.

[25]  P. Mcgeer,et al.  DISTRIBUTION OF TYROSINE HYDROXYLASE IN HUMAN AND ANIMAL BRAIN 1 , 1971, Journal of neurochemistry.

[26]  Cremer.  Chromatographie in der Gasphase , 1962 .

[27]  P. Riederer,et al.  Longevity in Parkinson's disease treated with L-DOPA , 1974 .

[28]  J. Davis,et al.  Relation of sex and aging to monoamine oxidase activity of human brain, plasma, and platelets. , 1971, Archives of general psychiatry.

[29]  O. Hornykiewicz,et al.  l-DOPA treatment in Parkinson's disease: Effect on dopamine and related substances in discrete brain regions , 1971, Experientia.

[30]  P. Riederer,et al.  The daily rhythm of HVA, VMA, (VA) and 5-HIAA in depressionsyndrom , 2005, Journal of Neural Transmission.

[31]  O. Hornykiewicz,et al.  Verteilung des 5-Hydroxytryptamins (Serotonin) im Gehirn des Menschen und sein Verhalten bei Patienten mit Parkinson-Syndrom , 1961, Klinische Wochenschrift.

[32]  W. B. Quay.  Circadian and Estrous Rhythms in Pineal Melatonin and 5-Hydroxy Indole-3-Acetic Acid.∗ , 1964, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

[33]  D. Joyce.  Changes in the 5-hydroxytryptamine content of rat, rabbit and human brain after death. , 1962, British journal of pharmacology and chemotherapy.

[34]  P. Riederer,et al.  The potentiation of the anti akinetic effect after L-Dopa treatment by an inhibitor of Mao-B, deprenil , 2005, Journal of Neural Transmission.

[35]  P. Riederer,et al.  [Biochemical findings in the brain in endogenous depression]. , 1975, Wiener medizinische Wochenschrift.

[36]  A. Lajtha,et al.  Postmortem changes in the cerebral free amino acid pool. , 1974, Brain research.

[37]  M. Hyyppä,et al.  Effect of L-dopa on brain monoamines and their metabolites in Parkinson's disease. , 1971, Life sciences. Pt. 1: Physiology and pharmacology.

[38]  A. Carlsson,et al.  Postmortal accumulation of 3-methoxytyramine in brain , 2004, Naunyn-Schmiedeberg's Archives of Pharmacology.

[39]  Sidney Udenfriend,et al.  Fluorescence assay in biology and medicine , 1962 .

[40]  P. Riederer,et al.  The balance of biogenic amines as condition for normal behaviour , 2005, Journal of Neural Transmission.

[41]  M. Sandler,et al.  IS THERE AN INCREASE IN MONOAMINE-OXIDASE ACTIVITY IN DEPRESSIVE ILLNESS? , 1975, The Lancet.

[42]  E. Anderson,et al.  The effect of a number of central depressant drugs upon brain 5-hydroxytryptamine levels in the rat. , 1962, The Journal of pharmacology and experimental therapeutics.

[43]  A. Carlsson,et al.  On the presence of 3-hydroxytyramine in brain. , 1958, Science.

[44]  Å. Bertler,et al.  A method for the fluorimetric determination of adrenaline and noradrenaline in tissues. , 1958, Acta physiologica Scandinavica.

[45]  I. Black,et al.  Postmortem changes in brain catecholamine enzymes. , 1975, Archives of neurology.

[46]  P. Riederer,et al.  Biochemical post-mortem findings in depressed patients , 2005, Journal of Neural Transmission.

[47]  L. Butcher,et al.  Behavioral and biochemical effects of L-dopa after peripheral decarboxylase inhibition. , 1969, Brain research.

[48]  K. Lloyd,et al.  Regional distribution of catecholamines in rat brain after L-3-O-methyldopa and L-dopa. , 1974, Life sciences.

[49]  A. Reinberg.  ASPECTS OF CIRCANNUAL RHYTHMS IN MAN , 1974 .

[50]  S. Snyder,et al.  Antiparkinsonian Drugs: Inhibition of Dopamine Uptake in the Corpus Striatum as a Possible Mechanism of Action , 1969, Science.

[51]  G M Everett,et al.  L-Dopa: Effect of Concentrations of Dopamine, Norepinephrine, and Serotonin in Brains of Mice , 1970, Science.

[52]  P. Riederer,et al.  Nucleus ruber and L-Dopa psychosis: Biochemical post-mortem findings , 2005, Journal of Neural Transmission.