Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:BIOD00035 (CSF)
 30,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebrospinal fluid gamma-aminobutyric acid (CSF GABA) was analyzed in 151 patients who underwent evaluation for central nervous system disease. CSF GABA was not detected in 19 of these patients, who had no evidence of neurologic disease and who served as controls. GABA was most frequently detected in patients with cerebrovascular disease, and was detected only in Parkinson's syndrome of atherosclerotic origin and dementia of multi-infarct type. CSF GABA was not detected in Alzheimer's disease or Huntington's disease. Patients with grand mal seizures exhibited CSF GABA elevation within 24 hours of the ictus. In patients with multiple sclerosis GABA detection was related to the presence or exacerbation of spinal cord lesions. Further study is necessary to evaluate the significance of elevated CSF GABA in central nervous system disease.
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PMID:Cerebrospinal fluid gamma-aminobutyric acid in neurologic disease. 13 99

Neuropathologically, Huntington's disease is characterized by a profound reduction in neuronal cells originating in the corpus striatum and globus pallidus. Since one of these cell types utilizes gamma-aminobutyric acid (GABA) as a neurotransmitter, it may be possible to differentially diagnose this disorder on the basis of the CSF content of this amino acid. In order to determine the validity of this hypothesis, cerebrospinal fluid GABA was analyzed, using a recently developed radioreceptor assay procedure and was found to be significantly reduced in patients diagnosed as having Huntington's disease and also lower in patients with Alzheimer's disease, though no difference was noted between Parkinson patients and control subjects. The results suggest that analysis of cerebrospinal fluid GABA may have diagnostic, and perhaps predictive, value in certain neurological disorders.
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PMID:Cerebrospinal fluid gamma-aminobutyric acid variations in neurological disorders. 14 28

In a large autopsy series of elderly individuals, organic dementia was attributed to (pre-) senile atrophy in 52.8%, to cerebrovascular disease in 22.5%, while 13.6% were of mixed senile and vascular origin, and 1.3% showed communicating hydrocephalus with meningopathies or were of undetermined origin. A survey is given of the morphological criteria of dementia resulting from disorders of cerebral blood supply and CSF circulation. The anatomic basis of vascular dementias are: atherosclerotic encephalopathy with lacunar state or multiple infarcts; granular cortical atrophy resulting from local microcirculation disorders; hypertensive cerebrovascular disease with the common "mixed" cortico-subcortical type, and the rare Binswanger's subcortical type. Atypical cerebral hemorrhage in old individuals rather results from congophilic (amyloid) angiopathy than from hypertensive arteriosclerosis. Multiple infarct dementia may also result from thrombotic microangiopathy, thromboembolic disease or cerebral vasculitides. The anatomical features of dementia associated with communicating "normal-pressure" hydrocephalus (NPH) are meningopathy at the basis or on the convexity, and fibrosis of the choroid plexus and/or arachnoid villi of post-inflammatory or undetermined origin, and other non-specific changes (periventricular gliosis). This condition is also associated with hypertensive cerebrovascular disease and Alzheimer's disease. Cerebral biopsies in NPH as well as in other types of hydrocephalus show enlarged extracellular spaces with otherwise normal neuropil probably resulting from increased transcapillary filtration. In some cases of "idiopathic" NPH no causative anatomical changes are found. The relationship between cerebral tissue changes, abnormal blood and CSF dynamics in these conditions remains to be clarified.
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PMID:Neuropathological aspects of dementias resulting from abnormal blood and cerebrospinal fluid dynamics. 96 75

Neuropeptide Y, one of the most abundant polypeptides within the nervous system, is co-stored with catecholamines, especially norepinephrine (NE), thus suggesting its possible involvement in pathologies characterized by a noradrenergic impairment. In Parkinson's disease (PD), as well as in multiple system atrophy (MSA), a central noradrenergic deficit has been demonstrated, and in the dementia of Alzheimer type (DAT) an impaired noradrenergic transmission has been postulated. In this study we determined CSF NE and MHPG levels in 29 PD, 15 MSA, 22 DAT patients and in 36 controls, while CSF NPY-immunoreactivity (NPY-ir) levels were measured in 10 PD, 7 MSA, 10 DAT patients and 20 controls. PD, MSA, and DAT patients showed a significant reduction in CSF NPY-ir and NE levels compared with controls, while CSF MHPG levels resulted in a reduction in only the MSA group. Furthermore, an inverse correlation between either NE or MHPG levels and the duration of the orthostatic hypotension was found in MSA patients while for DAT patients the MHPG levels were directly correlated to the severity of cognitive impairment, and inversely to the duration of illness.
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PMID:Cerebrospinal fluid norepinephrine, 3-methoxy-4-hydroxyphenylglycol and neuropeptide Y levels in Parkinson's disease, multiple system atrophy and dementia of the Alzheimer type. 132 Aug 91

An association between Alzheimer's Disease (AD) and low CSF and serum vitamin B12 (B12) has recently been described (1, 2, 3). This is apparently independent of nutritional intake (4). It has been suggested that such patients may exhibit an atypical form of cobalamin deficiency (3, 4). It is therefore proposed that these deficiencies may be aetiologically important, at least in sub-groups of AD, and a mechanism is described whereby B12 deficiency may result in the characteristic neurotransmitter changes of the disease. The hypothesis generates predictions regarding biochemical evaluation of such patients and suggests associations between the neurochemical disturbances and structural abnormalities of AD.
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PMID:Alzheimer's disease: a 'cobalaminergic' hypothesis. 1629 95

The modifications in the CSF content of glutamate and GABA in patients afflicted with primary degenerative dementia (PDD) and olivo-ponto-cerebellar atrophy (OPCA) have been evaluated. Control subjects (with disk herniation) were also included in the study. The amino-acids assays were carried out utilizing enzymatic-bioluminescence technique. GABA levels in controls were 803 +/- 98 (n = 7) and in demented patients 702 +/- 98 (n = 7) pmol/ml. Glutamate levels were 2067 +/- 244 (n = 10) in controls, 1190 +/- 81 (n = 16) pmol/ml (vs controls p less than 0.01) in demented patients, and 1116 +/- 146 (vs controls p less than 0.01) in OPCA patients. These results suggest that CSF glutamate levels in severely demented patients might be a result of generalized neuronal loss in the brain with a reactive gliosis.
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PMID:Glutamate and GABA levels in CSF from patients affected by dementia and olivo-ponto-cerebellar atrophy. 135 49

Previous investigators have detected unknown oxidized forms of 5-hydroxytryptamine (5-HT) in the CSF of Alzheimer's disease (AD) patients. Furthermore, an unidentified autoxidation product of this neurotransmitter is an inhibitor of acetylcholinesterase (AChE), an enzyme compromised in the Alzheimer brain. In this study it is demonstrated that the major product of autoxidation of 5-HT is 5,5'-dihydroxy-4,4'-bitryptamine (DHBT). Central administration of DHBT to mice at a dose of 40 micrograms (free base) evokes profound behavioral responses, which persist until the animals die (approximately 24 h). One hour after central administration of DHBT, the levels of norepinephrine, dopamine, 5-HT, and acetylcholine and their metabolites in whole brain are greatly elevated. Disturbances to the catecholaminergic and serotonergic systems were still evident shortly before the death of animals. DHBT is also shown to be a noncompetitive inhibitor of AChE in vitro. These observations suggest that if DHBT is formed as an aberrant metabolite of 5-HT in the human brain, it could potentially be neurotoxic and contribute to the neuronal degeneration and other neurochemical and neurobiochemical changes associated with AD or perhaps other neurodegenerative diseases.
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PMID:5,5'-Dihydroxy-4,4'-bitryptamine: a potentially aberrant, neurotoxic metabolite of serotonin. 135 95

We used the ELISA to measure the concentration of amyloid protein precursor with Kunitz type trypsin inhibitor domains (APPI) in CSF of dementia of the Alzheimer type (DAT) and examined the correlation of APPI with acetylcholinesterase (AChE) and somatostatin (SRIF). We found the APPI concentration in CSF of DAT to be significantly elevated compared with that of multi-infarct dementia and controls. We could significantly correlate APPI with AChE, but not correlate APPI with SRIF. The present results suggest that measurement of CSF APPI levels may be useful for diagnosis of DAT and the change of APPI may closely be associated with abnormality of acetylcholine system in DAT that has been reported.
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PMID:Amyloid beta protein precursors with kunitz-type inhibitor domains and acetylcholinesterase in cerebrospinal fluid from patients with dementia of the Alzheimer type. 137 55

31 cases of dementia of the aged were studied with the method of CSF cytology. Of the 31 cases, 14 were of Alzheimer dementia (AD), 17 multi-infarct dementia (MID), and 25 aged subjects were studied as control. The results showed that the number of lymphocytes in the CSF in AD group was obviously higher than that in MID group. The number of monocyte--macrophages was decreased in both two studied groups in comparing with that of the control group. We didn't find macrophages in AD group. The number of neutrophils in the CSF was high in both observed groups, and more markedly in AD group. The significance and specialty of the results need further study.
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PMID:[A preliminary study of cerebrospinal fluid cytology in aged patients with dementia]. 139 43

Cerebrospinal fluid concentrations of corticotropin-releasing hormone (CRH), thyrotropin-releasing hormone (TRH) and somatostatin (SRIF) were measured in 77 female inpatients with moderate to extreme dementia and in 17 elderly female controls. Both multi-infarct (MID) and Alzheimer-type (SDAT) demented patients had equally elevated CSF CRH and TRH but not SRIF levels as compared with the controls. This elevation was, however, not seen in patients with simple dementia while it was most prominent in those exhibiting marked depressive symptoms. It is concluded that depression rather than dementia itself may be associated with CSF CRH and TRH elevation in elderly patients with cognitive impairment.
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PMID:Cerebrospinal fluid neuropeptides in dementia. 148 50


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