Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A procedure is described for the rapid determination of the major indoles and catechols. Analysis with picogram detection limits was done by high-pressure liquid chromatography on a C18 reverse-phase column using electrochemical detection (LCEC). This method provides a comprehensive list of compounds which can be simultaneously determined in brain samples and for which there is no necessity of derivatization or pre-column purification. The regional distribution of 9 neurochemicals from rat brain and the levels of 10 neurochemicals from human brain are presented. DOPA, TYR, NE, MHPG, DOPAC, 5-HIAA, TRP, DA, HVA, 3-MT and 5-HT were detected in the caudate nucleus and putamen. The levels of neurochemicals from the caudate and putamen of a demented patient with Parkinson's disease were variably decreased; catechol and indole losses were greatest in the putamen. The levels of neurochemicals in the caudate and putamen of patients with Alzheimer's disease (SDAT) were also variably decreased; loss of NE was seen only in putamen and losses of DA, HVA and 5-HT were uniform across both caudate and putamen. The CSF of SDAT patients showed changes in NE only.
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PMID:Determination of tyrosine, tryptophan and their metabolic derivatives by liquid chromatography-electrochemical detection: application to post mortem samples from patients with Parkinson's and Alzheimer's disease. 396 72

The amine metabolites HVA and 5-HIAA in the lumbar CSF of 15 patients with Huntington's chorea were determined. A negative correlation was found between the severity of symptoms and the CSF HVA, but not 5-HIAA levels. The mean HVA concentration was lower than that of a group of patients with miscellaneous neurological disorders, similar to that of a group with miscellaneous psychiatric disorders and higher than that of a group with Parkinson's disease. The mean 5-HIAA concentration was similar to that of the neurological group and higher than those of the groups with psychiatric disorders or Parkinson's disease. CSF HVA and 5-HIAA concentrations of a single patient with severe akinetic rigid Huntington's chorea were similar to those found in Parkinson's disease. The findings are discussed in relation to previous neuropathological observations and to reported effects of drugs on the choreic symptoms.
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PMID:Amine metabolites in the cerbrospinal fluid in Huntington's chorea. 426 57

In 39 parkinsonian patients, CSF somatostatin content was 88.0 +/- 4.1 pg per milliliter, which was about 40% less than in controls (147.3 +/- 5.1 pg per milliliter). Somatostatin values were unrelated to age, sex, body weight, total CSF protein, immunoglobulin, or cell count in either group. Parkinsonian values were not related to duration of disease, severity, specific signs, or treatment. In contrast to multiple sclerosis, in which CSF somatostatin is low only during relapses, the low somatostatin content of CSF in Parkinson disease seems to be irreversible, to be present at the onset of symptoms, and to imply an irreparable functional or structural alteration of somatostatin-secreting neurons.
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PMID:Low cerebrospinal fluid somatostatin in Parkinson disease: an irreversible abnormality. 612 3

Studies have previously demonstrated low somatostatin levels in autopsy cortical tissue from Alzheimer's disease (AD) patients and low somatostatin levels in CSF obtained from subjects with dementia. We evaluated levels of this peptide in 21 non-depressed subjects, 10 with AD, 2 with Parkinson's disease (PD), and 9 with other neurological conditions. The AD patients had significantly lower mean CSF somatostatin than the "other" neurological patients (14.6 +/- 1.5 S.E.M. versus 26.7 +/- 3.2 pg/ml, p less than 0.005). A demented PD subject had a level in the range of the AD group, while the non-demented PD patient had a value above this range. Thus, all 11 patients with AD or PD dementia, analogous disorders, had levels below 21.8 mg/ml, while 7 of the 10 remaining patients had values above 21.8 pg/ml. Age did not explain this finding.
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PMID:CSF somatostatin in Alzheimer's disease. 615 Nov 23

To determine whether 1-tyrosine administration can enhance dopamine synthesis in humans as it does in rats, we measured levels of tyrosine and the major dopamine metabolite, homovanillic acid, in lumbar spinal fluids of 23 patients with Parkinson's disease before and during ingestion of 100 mg/kg/day of tyrosine. Nine patients took 100 mg/kg/day of probenecid in six divided doses for 24 hours prior to each spinal tap; 14 patients did not receive probenecid. L-tyrosine administration significantly increased CSF tyrosine levels in both groups of patients (p less than .01) and significantly increased homovanillic acid levels in the group of patients pretreated with probenecid (p less than .02). These data indicate that l-tyrosine administration can increase dopamine turnover in patients with disorders in which physicians wish to enhance dopaminergic neurotransmission.
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PMID:Effects of oral L-tyrosine administration on CSF tyrosine and homovanillic acid levels in patients with Parkinson's disease. 617 72

Depression is a common symptom in patients with Parkinson's disease. It is not related to the severity of the motor symptoms or changes in dopamine metabolism and does not improve on treatment with dopamine agonists. Alterations in serotonin metabolism are found in primary (endogenous) depression. The brain content of serotonin in Parkinson's disease is also reduced, but this has not been related to any manifestation of the disorder. We found that the CSF content of the major metabolite of serotonin, 5-hydroxyindoleacetic acid, was lower in depressed than in nondepressed parkinsonians. The data suggest that the alterations in serotonin metabolism in Parkinson's disease identify a subgroup of patients who are prone to depression.
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PMID:Altered serotonin metabolism in depressed patients with parkinson's disease. 620 Aug 1

Recently established standardized protocols for collection, handling, and storage of CSF for measurement of gamma-aminobutyric acid (GABA) have proven valuable in the characterization of various CNS disorders. In response to two recent reports which may have an impact on certain widely used protocols, we have, using the confirmed ion-exchange/fluorometric procedure, systematically evaluated the effects of deproteinization with various concentrations of sulfosalicylic acid (SSA) ranging from 0 to 10% (100 mg/ml), as well as the effects of freeze/thaw (F/T) on CSF GABA levels. Results of F/T studies documented that levels are stable to freezing and thawing. Acid deproteinization studies revealed the presence of an equilibrium between strictly free GABA, demonstrable only in acid-free CSF, and a very loosely bound form of GABA, fully demonstrable only in CSF deproteinized with concentrations of SSA above 1% (10 mg/ml). The relationship between GABA concentrations in undeproteinized and acid-deproteinized CSF revealed a highly significant (p less than .001) correlation, suggesting that alterations of central GABAergic activity would be reflected by either the level of strictly free GABA or free plus loosely bound GABA. This hypothesis was upheld in studies of patients with Parkinson's disease (PD) and Huntington's disease (HD), two neurologic disorders in which dysfunctions of the GABA system have been implicated. Results indicated that CSF GABA levels are significantly reduced in both PD and HD patients compared with neurologically normal controls, whether the measurement is of free GABA or free plus loosely bound GABA. Thus, we conclude that the level of strictly free GABA is stable to freezing and thawing and can only be accurately determined in nonacidified CSF; however, existing protocols employing deproteinization in 5% SSA yield data that provide an equally good reflection of central GABAergic transmission.
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PMID:Further characterization of in vitro conditions appropriate for GABA determination in human CSF: impact of acid deproteinization and freeze/thaw. 622 37

gamma-Aminobutyric acid (GABA) was measured in CSF as such and following acid hydrolysis by the ion-exchange/fluorometric method. The conjugated GABA level was obtained by subtracting the free GABA level from the total GABA level. Results showed that at room temperature, while the free GABA level increased, the level of conjugated GABA decreased in a linear fashion during the first 24 h (r = -0.974; P less than 0.001). Aging and CSF conjugated GABA levels were inversely correlated (r = -0.613; P less than 0.05). Unlike free GABA levels, the levels of conjugated GABA were not altered in Huntington's disease, Parkinson's disease, cerebellar ataxias, dementias, epilepsy and multiple sclerosis compared to controls. In patients with Huntington's disease, on administration of isoniazid at 900 mg/day, along with pyridoxine at 100 mg/day, a 4-fold increase of both free (P less than 0.005) and conjugated GABA (P less than 0.0025) was seen. The results indicate that while total GABAergic peptides are not altered in several of the neurologic diseases studied, drugs such as isoniazid and/or pyridoxine can significantly elevate both free and conjugated GABA levels in human CSF.
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PMID:Free and conjugated GABA in human cerebrospinal fluid: effect of degenerative neurologic diseases and isoniazid. 623 93

Antibodies against herpes simplex virus (HSV) types 1 and 2 and cytomegalovirus (CMV) were assayed with a microindirect hemagglutination (IHA) test in the serum of 67 pairs of patients with Parkinson's disease and controls. Cerebrospinal fluid from 30 pairs was assayed. All patient and control serum was tested with a radioimmunoassay (RIA) for antibodies against HSV type 1 subunit antigens. Serum IHA antibody level against HSV type 1 was increased in patients with Parkinson's disease and RIA antibody levels against the same viral antigen were significantly higher in the patients than controls. Herpes simplex virus type 2 and CMV serum antibodies were equal in the patient and control groups. Most of the CSF samples tested negatively for IHA; small and comparable numbers of the patients and controls had low antibody levels against HSV and CMV antigens.
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PMID:Herpesviruses and parkinsonism. Herpes simplex virus types 1 and 2, and cytomegalovirus antibodies in serum and CSF. 625 11

Serum and cerebrospinal fluid (CFS) immunoglobulin G (IgG) antibodies to herpes simplex (HSV) and measles viruses were assayed with a radioimmunoassay in 56 patients with idiopathic Parkinson's disease and in a similar number of age- and sex-matched controls with other neurological diseases. As a group, the patients with Parkinson's disease had a significantly increased serum antibody level against HSV, but measles virus antibody levels were similar in both groups. Both in the Parkinson's group and in the control group, the levels of the total IgG in CSF were within normal limits and the CSF antibodies to HSV and measles virus paralleled the serum antibody titers relative to the total IgG serum-to-CSF ratios. This indicates no increased intrathecal antibody production in either group. In 48 patients with Parkinson's disease who were HLA-typed, no association of viral antibody levels with particular HLS antigens were noted. The findings suggest that HSV is not present within the central nervous system of the patients with Parkinson's disease. The increase HSV antibody level seen in Parkinson's disease patients may reflect a more general disturbance of the patients' immune functions.
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PMID:Virus antibodies in Parkinson's disease. Herpes simplex and measles virus antibodies in serum and CSF and their relation to HLA types. 628 83


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