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 patient with Parkinson's disease developed a non-ketotic hyperosmolar diabetic coma precipitated by chest infection. Initial improvement from treatment with intravenous insulin, ampicillin and fluid therapies was followed by severe deterioration and hypovolaemic shock. Further improvement occurred only when therapy directed against Gram-negative sepsis was added. A barium examination later demonstrated aspiration of oral contents with pulmonary soilage. The differences between the easily recognized early fulminating 'aspiration syndrome' caused by aspiration of gastric contents of low pH and the aspiration of oral contents, which may remain occult for many hours, is highlighted. Life-threatening Gram-negative or anaerobic infection may then occur but remain undiagnosed because the original aspiration of foreign material is unsuspected.
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PMID:Aspiration of oral contents in Parkinson's disease. A case report. 403 2

Tissue from human fetal cadavers has long been used for medical research, experimental therapies, and various other purposes. Research within the last two decades has led to substantial progress in many of these areas, particularly in the application of fetal tissue transplantation to the treatment of human disease. As a result, clinical trials have now been initiated at centers around the world to evaluate the use of human fetal tissue transplantation for the therapy of Parkinson's disease, insulin-dependent diabetes mellitus, and a number of blood, immunological and, metabolic disorders. Laboratory studies suggest a much wider range of disorders may in the future be treatable by transplantation of various types of human fetal tissue. A combination of characteristics renders fetal tissue uniquely valuable for such transplantation, as well as for basic research, the development of vaccines, and a range of other applications. Although substitutes for human fetal tissue are being actively sought, for many of these applications there are at present no satisfactory alternatives. Important issues remain unresolved concerning the procurement, distribution, and use of human fetal cadaver tissue as well as the effects of such use on abortion procedures and incidence. These issues can be addressed by the introduction of appropriate guidelines or legislation, and need not be an impediment to legitimate research and therapeutic use of fetal tissue.
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PMID:Human fetal tissue research: practice, prospects, and policy. 801 29

Immunohistochemistry using both a newly developed polyclonal, and a commercially available monoclonal, anti-insulin receptor antibody was done on the midbrain from cases of idiopathic Parkinson's disease (PD), Alzheimer's disease, amyotrophic lateral sclerosis, vascular parkinsonism and non-neurological controls. Both antibodies gave identical patterns of neuronal staining. The neurons of the oculomotor nucleus were immunopositive in all the brains. However, the neurons in the pars compacta of the substantia nigra, paranigral nucleus, parabrachial pigmental nucleus, tegmental pedunculopontine nucleus, supratrocheal nucleus, cuneiform nucleus, subcuneiform nucleus and lemniscus medialis, which were positive in other diseases and in non-neurological controls, were not stained by these antibodies in PD brains. These results suggest that, in PD, a dysfunction of the insulin/insulin receptor system may precede death of the dopaminergic neurons.
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PMID:Loss of insulin receptor immunoreactivity from the substantia nigra pars compacta neurons in Parkinson's disease. 801 69

It has been reported that 50% to 80% of patients with Parkinson's disease have abnormal glucose tolerance which may be further exacerbated by levodopa therapy. Little is known about the impact of chronic hyperglycemia on the severity of the motor manifestations and the course of the disease as well as its impact on the efficacy of levodopa or other dopaminergic drugs. This issue, which has been largely ignored, is of clinical relevance since animal studies indicate that chronic hyperglycemia decreases striatal dopaminergic transmission and increases the sensitivity of postsynaptic dopamine receptors. In addition, evidence from experimental animal studies indicates that diabetic rats are resistant to the locomotor and behavioral effects of the dopamine agonist amphetamine. The resistance to the central effects of amphetamine is largely restored with chronic insulin therapy. In the present communication, I propose that in Parkinson's disease diabetes may exacerbate the severity of the motor disability and attenuate the therapeutic efficacy of levodopa or other dopaminergic agents as well as increase the risk of levodopa-induced motor dyskinesias. Thus, it is advocated that Parkinsonian patients should be routinely screened for evidence of glucose intolerance and that if found aggressive treatment of the hyperglycemia may improve the response to levodopa and potentially diminish the risk of levodopa-induced motor dyskinesias.
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PMID:The relationship between diabetes mellitus and Parkinson's disease. 808 98

To clarify the incidence and risk factor of postprandial hypotension (PPH) in Parkinson's disease, a 75g oral glucose tolerance test (OGTT) was carried out in 23 patients (Hoehn-Yahr score II in 2, III in 18 and IV in 3) without postprandial symptoms. We defined the patients whose systolic blood pressure fell more than 20 mmHg during the 75g OGTT as group I and less than 20 mmHg as group II. In 14 patients with Parkinson's disease (61%), the systolic blood pressure fell more than 20 mmHg without symptoms. There were no significant differences in in age, disease duration, clinical stage or antiparkinsonian drug between groups I and II. However, the baseline systolic and diastolic blood pressures were significantly higher in group I than in group II. In group I patients, the maximum decrease in systolic blood pressure was seen after more than 60 minutes and serum insulin response was higher than in group II patients from 60 to 120 min. Systolic blood pressure declined accompanied by the rise of insulin. These results suggest that PPH occurs at high incidence in patients with moderately severe Parkinson's disease, and that high baseline blood pressure and abnormally high insulin response to glucose load may play a role, while medications for Parkinson's disease may not.
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PMID:[Postprandial hypotension in Parkinson's disease--the incidence and risk factor]. 812 70

The first disease due to disturbances in a cell organelle was discovered in 1959-62, and its basis was loose-coupling of oxidative phosphorylation in the skeletal muscle mitochondria accompanied by severe alterations of their structure (Luft's disease). During the 1980s, functional disturbances and structural alterations in the mitochondria were observed in more than 100 disease entities, mainly in parts of the central nervous system and skeletal muscles. A second breakthrough in this area was the discovery in 1963-64 that mitochondria had their own DNA, mtDNA. Following the observation in 1988 of mutations of mtDNA in mitochondrial diseases, such mutations--mainly deletions and point mutations--were observed in almost all mitochondrial diseases. A remarkable extension of the area is the notion that "normal" ageing is accompanied by decreased oxidative phosphorylation and the appearance of mtDNA mutations. During the last two years, such changes have been demonstrated in diseased states in tissues and organs, which are especially reliant on oxygen supply: in the central nervous system (Parkinson's disease, some types of epilepsy and seizures, Huntington's disease, possibly also in Alzheimer's disease); in heart muscle (cardiomyopathies) and in skeletal muscle. Type 2 diabetes or NIDDM engages two tissues most reliant on oxygen consumption, the pancreatic islets (insulin secretion) and skeletal muscle (insulin sensitivity). Both these functions are genetically determined, the latter to a high degree also controlled by "environmental" factors. The evident age factor in the development of NIDDM could be on a par with the "normal" ageing process.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Physiopathology of mitochondria. From Luft's disease to aging and diabetes]. 836 14

We investigated the effect of a balanced liquid meal on blood pressure (BP) and heart rate (with patients supine and during head-up tilt), and on levels of plasma catecholamines, glucose, and insulin, in patients with idiopathic Parkinson's disease (IPD), multiple system atrophy (MSA), pure autonomic failure (PAF), and in healthy subjects (controls). After food, supine BP fell in IPD, but to a greater extent in MSA and PAF. In controls, BP was unchanged. Head-up tilt did not lower BP in IPD and controls, but there was a postprandial fall to lower levels in both MSA and PAF. Plasma norepinephrine levels rose in IPD pre- and postprandially during tilt, but were unchanged in MSA and PAF. These data suggest that in IPD, food causes a smaller fall in supine BP than in MSA and PAF. In IPD, as in controls, food does not induce or unmask postural hypotension, unlike in MSA and PAF, in which BP falls to even lower levels. There are therefore differences in the responses to food ingestion between these groups. This may be of value in separation of these disorders at an early stage.
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PMID:Cardiovascular and hormonal responses to liquid food challenge in idiopathic Parkinson's disease, multiple system atrophy, and pure autonomic failure. 849 45

Apomorphine is a D1 and D2 dopamine receptor agonist with anti-parkinsonian properties qualitatively similar to those seen with L-dopa. It was first used in the treatment of Parkinson's disease by Schwab in the 1950s but owing to its short duration of action, the need for parenteral administration, and adverse reactions including nausea, vomiting, postural hypotension and sedation, it was not widely prescribed. In the early 1970s, Cotzias confirmed its potent anti-parkinsonian effects and that some of its secondary effects were diametrically opposite to those seen with L-dopa. The advent of peripheral dopamine receptor antagonist drugs, which counteract the unwanted effects of apomorphine, and the development of new drug delivery systems including insulin pens and ambulatory mini pumps have led to the resurrection of apomorphine for the treatment of Parkinson's disease. Over the last five years in Europe, the drug has proved to be a major advance in the treatment of refractory "on-off" oscillations in Parkinson's disease. It has also been used as a diagnostic test for dopaminergic responsiveness in Parkinson syndromes and tremors of uncertain aetiology. The drug has also proved particularly useful in dealing with certain "off-period" disabilities, including pain, bladder dysfunction, dystonia and gastro-intestinal symptoms. Continuous steady state infusion of apomorphine by mini-pump may reduce the severity of "on" phase dyskinesias over time. The drug has also proved useful in the clinical pharmacological investigation of the pathophysiology of the motor response to dopaminergic drugs in Parkinson's disease and the occurrence of involuntary movement sequences. Neuropsychiatric side-effects are relatively infrequent when compared with ergolene dopamine agonists.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dopamine agonists in Parkinson's disease: a look at apomorphine. 850 Jul 83

An ATP-sensitive potassium channel (KATP) is known to modulate insulin release from pancreatic beta cells. It has been proposed that potassium channels related to KATP in the nervous system might similarly modulate neurotransmitter release. We have therefore investigated the effects of KATP opening agents on GABA release in the globus pallidus. Diazoxide and cromakalim decreased the K(+)-evoked release of [3H]GABA from pallidal slices. The maximum inhibition observed for diazoxide (59%) and cromakalim (66%) was achieved at a concentration of 100 microM. The effects of both cromakalim and diazoxide were significantly antagonized by the concurrent application of the sulfonylurea glibenclamide (100 microM). Intrapallidal injections of diazoxide in the reserpine-treated rat model of Parkinson's disease reduced akinesia in a dose-dependent manner. These data suggest that manipulation of neuronal potassium channels with pharmacological properties similar to KATP may prove useful in the treatment of Parkinson's disease.
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PMID:Modulation of GABA transmission by diazoxide and cromakalim in the globus pallidus: implications for the treatment of Parkinson's disease. 863 58

At present, search for the causes of neurodegenerative diseases represents a major topic in brain research. Acquired disturbances of cell metabolism are supposed to be a cause of the two most important neurodegenerative disorders in ageing, like senile dementia of the Alzheimer type and Parkinson's disease, resulting in measurable decreases of in vivo and post mortem cerebral glucose metabolism. Accumulating evidence indicates that insulin plays an important role in the regulation of brain glucose homeostasis in the central nervous system and has trophic effects on neurons. It has been suggested that the reduction of brain glucose metabolism in neuro-degenerative disorders may be related to a defect of the neuronal insulin-insulin receptor-interaction. It will be the aim of our study to demonstrate whether there exist any changes in the content of insulin, its receptor and/or in the functionality of the insulin receptor and its signal transduction in neurodegenerative disorders as Alzheimer's and Parkinson's disease.
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PMID:Altered regulation of brain glucose metabolism as a cause of neurodegenerative disorders? 882 Oct 49


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