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)

Several factors place older patients at increased risk for malnutrition. The physiologic effects of aging itself are considered risk factors, as are systemic diseases such as Parkinson's disease, diabetes, infection, and cancer; depression, and other psychiatric disorders; abnormal chemical values; and effects of various medications. Many of these factors are reversible if recognized and assessed early. Cholesterol and albumin measurements may help confirm the diagnosis of malnutrition. Nutrition-promoting interventions that you can recommend include increasing exercise, raising levels of fluid and nitrogen intake, avoiding constipation through dietary and lifestyle changes, and recommending routine dental examinations.
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PMID:The malnourished older patient: when and how to intervene. 832 14

Transforming growth factor (TGF)beta plays a role in injury repair in sites surrounding brain injury. The present study tested the hypothesis that TGFbeta1 and TGFbeta2 levels in the postmortem CSF of patients with neurodegenerative disorders would be elevated compared to those in normal subjects. Free TGFbeta1 and total TGFbeta2 were measured by ELISA in postmortem ventricular cerebrospinal fluid (vCSF) of patients with Parkinson's disease (n = 30), Alzheimer's disease (n = 30), multiple sclerosis (n = 15), and schizophrenia (n = 12) and of normal controls (n = 16). In addition, albumin, IgG, and total protein in vCSF were measured. Both TGFbeta1 and TGFbeta2 were significantly different between groups (P < 0.002 and P < 0.001, respectively). Parkinson's disease vCSF showed significant increases in both TGFbeta1 (P = 0.015) and TGFbeta2 (P = 0.012) compared to normal controls. There was a trend for TGFbeta2 to be elevated in Alzheimer's disease and multiple sclerosis vCSFs, which failed to achieve significance. There were no differences between controls and schizophrenics in TGFbeta1 or TGFbeta2. Alzheimer's disease vCSF showed a significant decrease in protein compared to all other groups, which was not related to blood-brain barrier permeability, age, or autolysis differences. Evidence is presented suggesting that some TGFbeta1 may leak into the vCSF from plasma. Autopsy vCSF levels of TGFbeta isoforms were found to be distinctly different from those reported for human serum, especially for TGFbeta2, which is undetectable in plasma. These results indicate that further in vivo studies of TGFbeta2 in the CSF of Parkinson's disease patients are warranted to determine the relationship between clinical status, medication, and TGFbeta2 concentrations.
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PMID:TGFbeta1 and TGFbeta2 concentrations are elevated in Parkinson's disease in ventricular cerebrospinal fluid. 893 62

Oxidative damage by free radicals may contribute to the etiology of Parkinson's disease (PD), and increased oxidative stress in the nigral cells of PD patients may occur following L-dopa treatment, prompting suggestions that L-dopa therapy should be delayed as long as possible. Bilirubin is a potent antioxidant in vitro, even when bound to albumin, suggesting a physiological role as an antioxidant. Calculations indicate that bilirubin can pass the blood-brain barrier in sufficient quantity to exert a significant antioxidant effect in the brain. We have found a highly significant (about 20%) increase in plasma bilirubin in 162 PD patients on chronic L-dopa treatment compared to 93 untreated parkinsonians and 224 non-parkinsonian controls. We propose that L-dopa-induced increase in nigral oxidative stress in PD may be effectively counteracted by increased bilirubin levels. The mechanism by which plasma bilirubin is increased in patients receiving L-dopa is at present unknown.
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PMID:Increased plasma bilirubin in Parkinson patients on L-dopa: evidence against the free radical hypothesis? 923 25

Electroconvulsive therapy (ECT) was given to 16 non-depressed, non-demented patients with advanced Parkinson's disease (PD). In all the patients an antiparkinsonian effect was seen, lasting for 18 months in one patient, 3-5 months in seven patients, and a few days to four weeks in eight patients. After ECT the levels of homovanillic acid and neuropeptide Y in cerebrospinal fluid (CSF) were significantly increased. The eight patients with long lasting motor improvement after ECT had significantly lower CSF-3-methoxy-4-hydroxyphenylglycol compared to the group with short lasting improvement. Five patients developed transitory mental confusion after ECT. In these patients, and in no others, a high albumin-ratio was found already before ECT was given - an indication of blood CSF barrier damage. Our results suggest that ECT is valuable in patients with drug refractory PD or PD with intolerance to antiparkinsonian drugs.
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PMID:ECT in Parkinson's disease. Changes in motor symptoms, monoamine metabolites and neuropeptides. 962 60

The purpose of this study was to investigate the relationship between weight loss and dysphagia in Parkinson's disease. We compared the height, body weight and the data of self-administered questionnaires concerning food intake and deglutition feelings in patients suffering from Parkinson's disease with normal controls. A structured interview was performed by nutritionists and nutrient intakes were calculated from the reported food intake over 5 days. Biochemical parameters were chosen from the chart. The subjects were 105 patients with Parkinson's disease, 34 males with a mean age of 67.7 +/- 8.6 years and 71 females with a mean age of 69.1 +/- 10.0 years (Hoehn-Yahr stage I6, II25, III51, IV20, V3). In addition, 47 family members were used as control subjects: 26 males, 70.6 +/- 7.6 years and 21 females, 64.9 +/- 7.7 years. Body mass index (BMI) in females with Parkinson's disease (20.2 +/- 3.5 kg/m2) was significantly lower (p < 0.005) than that in control females (23.0 +/- 3.0 kg/m2). There was no significant difference in BMI in males. The BMI was 21.9 +/- 3.0 kg/m2 in male patients with Parkinson's disease and 22.6 +/- 3.1 kg/m2 in controls. The occurrences of symptoms such as choking, cough, sputum, food in sputum, wet voice and pharyngeal discomfort following food intake in patients with Parkinson's disease vs. those in controls were 22% vs. 6%, 16% vs. 2%, 7% vs. 4%, 2% vs. 0%, 5% vs. 2% and 11% vs. 0%, respectively. Concerning symptoms such as choking, cough and pharyngeal discomfort, the occurrence was significantly more frequent in patients with Parkinson's disease than in controls (p < 0.05, p < 0.05, p < 0.05). We defined the dysphagic Parkinson patients as those who have at least one symptom of dysphagia such as choking, cough, sputum, food in sputum, wet voice and pharyngeal discomfort following food intake. The dysphagic subjects were present in 31% of Parkinson patients and in 7% of control subjects (p < 0.005), although half of the dysphagic Parkinson patients did not recognize it. No relationship between the occurrence of dysphagic symptoms and the Hoehn-Yahr stage was found. In patients with Parkinson's disease. BMI in the dysphagic group (19.1 +/- 3.6 kg/m2) was significantly lower than that in the non-dysphagic group (21.6 +/- 3.0 kg/m2) (p < 0.005). There was no relationship between BMI and the dose of levodopa. Patients in the dysphagic group showed significantly lower carbohydrate intake (186 +/- 49 g) than those in the non-dysphagic group (215 +/- 52 g) (p < 0.05). Biochemical nutritional parameters were lower in the dysphagic group than those in the non-dysphagic group; 6.6 +/- 0.7 g/dl vs. 6.9 +/- 0.4 g/dl (p < 0.005) in serum total protein, 3.8 +/- 0.5 g/dl vs. 4.1 +/- 0.4 g/dl (p < 0.01) in albumin and 173.4 +/- 33.0 mg/dl vs. 199.7 +/- 40.7 mg/dl (p < 0.05) in total cholesterol. These findings suggest that dysphagia, especially unrecognized dysphagia, plays a role in weight loss in Parkinson's disease.
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PMID:[Relationship between weight loss and dysphagia in patients with Parkinson's disease]. 1065 60

Neuromelanin is a dark brown pigment suspected of being involved in the pathogenesis of Parkinson's disease. This pigment can be isolated from normal human substantia nigra by a procedure that includes an extensive proteolytic treatment. In this study we used such a procedure to extract the neuromelanin pigment from a pool of substantia nigra from patients affected by Parkinson's disease. 13C Cross polarization magic angle spinning nuclear magnetic resonance spectroscopy and electron paramagnetic resonance spectroscopy were used to characterize the solid residue obtained from the extraction procedure. We found that the pigment extracted from the substantia nigra of parkinsonian patients was mainly composed of highly cross-linked, protease-resistant, lipo-proteic material, whereas the neuromelanin macromolecule appears to be only a minor component of this extract. A synthetic model of melanoprotein has been prepared by enzymatic oxidation of dopamine in the presence of albumin. Once it has undergone the same proteolytic treatment, this model system yields a 13C-NMR spectrum which is similar to that observed for the parkinsonian midbrain extract. These results are consistent with the view that oxidative stress has a relevant role in the pathogenesis of Parkinson's disease.
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PMID:Isolation and 13C-NMR characterization of an insoluble proteinaceous fraction from substantia nigra of patients with Parkinson's disease. 1100 8

Convection-enhanced delivery (CED) distributes macromolecules in the brain in a homogeneous, targeted fashion in clinically useful volumes. However, the binding of growth factors to heparin-binding sites in the extracellular matrix may limit the volume of distribution (V(d)). To overcome this limitation, we examined the effects of heparin coinfusion on V(d) of glial-derived neurotrophic factor (GDNF), neurturin (NTN), artemin, and a nonspecifically bound protein, albumin. Heparin coinfusion significantly enhanced the V(d) of GDNF and GDNF-homologous trophic factors, probably by binding and blocking heparin-binding sites in the extracellular matrix. Furthermore, coinfusion of heparin with NTN enhanced striatal dopamine metabolism, compared to trophic factor administered alone. The negligible benefit of GDNF in recent clinical trials of Parkinson's disease may result from limited tissue distribution. Heparin coinfusion during CED targeting the striatum may alleviate this important limitation. This study demonstrates the influence of receptor binding on the distribution of trophic factors in the CNS.
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PMID:Heparin coinfusion during convection-enhanced delivery (CED) increases the distribution of the glial-derived neurotrophic factor (GDNF) ligand family in rat striatum and enhances the pharmacological activity of neurturin. 1117 Jul 30

Dysfunction of the blood-cerebrospinal fluid barrier (BCB) has been implicated in the pathogenesis of Parkinson's disease (PD) and other neurodegenerative disorders. Therefore, we assayed serum and cerebrospinal fluid (CSF) from 30 parkinsonian patients and 30 controls for concentrations of albumin and IgG. The CSF/serum ratio for albumin (AQ), IgG (GQ), IgG-index as well as determination of oligoclonal bands were used to evaluate BCB function and to quantify humoral immune response within the central nervous system (CNS). Levels of AQ, GQ and IgG-index did not significantly differ in both groups. We found no dysfunction of the blood-CSF barrier or signs of local synthesis of IgG in the central nervous system of parkinsonian patients. Our data do not support the hypothesis of a dysfunctional BCB that contributes to pathophysiological mechanisms underlying PD.
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PMID:Integrity of the blood-cerebrospinal fluid barrier in early Parkinson's disease. 1122 41

Reactive oxygen species (ROS) generated from dopamine and its oxidation products have been implicated in the pathogenesis and toxicity from treatment of Parkinson's disease-associated autonomic neuropathy, and antioxidant therapies have been proposed as treatment and prophylaxis for this disorder. However, many antioxidants are rapidly and, under physiological conditions, irreversibly oxidized, rendering them redox-inactive. We have examined the potential of 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl and polynitroxylated albumin (TEMPOL/PNA), an antioxidant complex that facilitates recycling of inactivated antioxidant to its redox-active form, as a protective agent against the toxicity of the catecholaminergic ROS generator, 6-hydroxydopamine (6-OHDA). TEMPOL/PNA is more effective against depression of activity level by 6-OHDA than the non-recycling antioxidant, TEMPOL, in a murine model of catecholaminergic oxidative damage. TEMPOL/PNA is also less toxic than TEMPOL in mice, allowing administration of higher doses of antioxidant. Both TEMPOL and TEMPOL/PNA give rise to prevention of apoptosis and to translocation of NF-kappaB from the cytoplasm to the nucleus of PC12 cells treated with 6-OHDA, but in vivo, TEMPOL/PNA maintains redox-active blood levels of TEMPOL for almost 5 h, whereas administration of TEMPOL alone results in clearance of blood redox activity within 1 h. PNA enhances the therapeutic index of TEMPOL, and the recycling antioxidant that results from their adjunctive administration may prove useful in disorders involving oxidative stress.
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PMID:Prevention of catecholaminergic oxidative toxicity by 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl and its recycling complex with polynitroxylated albumin, TEMPOL/PNA. 1515 56

TEMPOL (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) is a stable nitroxyl antioxidant. Previous studies have suggested that TEMPOL is protective in acute disorders thought to involve reactive oxygen species (ROS), such as ischemic stroke and cardiac reperfusion injury. Oxidized TEMPOL can be recycled to its redox-active reducing form by co-administration with polynitroxylated albumin, making it a candidate as a pharmacological "reservoir" for reducing potential of use in chronic disorders involving ROS. The present studies examine the efficacy of TEMPOL in cell culture and animal models of the central and peripheral dysfunction associated with Parkinson's disease, a disorder in the pathogenesis of which ROS generated from dopamine have been implicated. Antioxidants have been proposed as both preventive and symptomatic therapy for Parkinson's disease. TEMPOL protects MN9D dopaminergic mesencephalic cells in culture from 6-hydroxydopamine (6-OHDA)-induced apoptosis. Translocation of the p65 component of NF-kappaB to the nucleus accompanies protection by TEMPOL. In vivo, intraperitoneal TEMPOL protects mice from intrastriatal 6-OHDA-induced cell and dopamine metabolite loss in the striatum. TEMPOL also protects mice against the 6-OHDA-induced rotational behavior elicited by intrastriatal administration of d-amphetamine. In addition, TEMPOL protects mice from the ptosis, activity level decrement, and mortality induced by intraperitoneal administration of 6-OHDA, a model of autonomic dysfunction in Parkinson's disease. Adjunctive use of polynitroxylated albumin enhances the in vitro and in vivo effects of TEMPOL.
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PMID:Neuroprotective effects of TEMPOL in central and peripheral nervous system models of Parkinson's disease. 1614 94


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