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

Zero concordance for Parkinson disease was found in the first 12 monozygotic twin pairs examined in an ongoing twin study. One co-twin (subject without Parkinson disease) had essential tremor, another had cerebral vascular disease, and a third was an alcoholic. Cigarette smoking appeared to be less frequent in the probands than in the co-twins (11.9 versus 16.1 pack-years). There was also evidence of premorbid personality differences between probands and co-twins dating back to late adolescence or early adult years. These preliminary findings suggest that genetic factors do not play a major role in the etiology of Parkinson disease and point to a prodromal onset of the disease as early as late adolescence or early adult life.
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PMID:Twin study of Parkinson disease. 719 28

A study of 100 Day Hospital patients showed that 26 elderly patients with mild Senile Parkinsonism and varying degrees of dementia had subclinical tremor with the same frequency as Parkinson's Disease and distinguishable by amplified recordings from those of Parkinson's Disease and Senile Tremor. A significant history of cerebro-vascular disease was obtained in one-half of these patients. The recording of tremor is shown to be of value in diagnosing Parkinsonism and in assessing response to treatment.
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PMID:Tremor and senile parkinsonism. 720 98

In order to assess qualitatively the sympathetic functions of the peripheral vessels, we performed a scintigraphical study of the entire body with meta-[123I]iodobenzylguanidine (MIBG) in 13 patients with autonomic failure and 11 healthy subjects as control. The patients comprised seven with multiple system atrophy (MSA), two with pure autonomic failure (PAF), three with Parkinson's disease with autonomic failure (PD with AF) and one with familial amyloid polyneuropathy (FAP). No clinical evidence of vascular disease was noted in any of the patients and the control subjects. We investigated their autonomic functions using the head up tilt test as well as norepinephrine and isoproterenol infusion tests. We found that: (i) All of the control subjects showed satisfactory MIBG uptake; (ii) all of the patients with PAF and FAP, most of whom had postganglionic sympathetic lesions, showed supersensitivity and low MIBG uptake; (iii) almost all the patients with MSA, who were considered to have mainly preganglionic sympathetic lesions, showed supersensitivity and diminished MIBG uptake, although the patients with olivopontocerebellar atrophy showed supersensitivity but not diminished MIBG uptake. In conclusion, these results suggest that peripheral vascular scintigraphy using MIBG is useful in detecting peripheral adrenergic dysfunction.
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PMID:A scintigraphical qualitative analysis of peripheral vascular sympathetic function with meta-[123I]iodobenzylguanidine in neurological patients with autonomic failure. 756 Jul 60

The Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) provides ratings of an individual's changes in everyday cognitive functions during the previous 10 years. Original studies conducted in Australia showed that its score was not influenced by the subjects' educational backgrounds and that it performed at least as well as the Mini-Mental State Examination (MMSE) as a screening instrument for dementia. The subjects of the present study were Chinese and included 399 community residents and 61 dementia patients. Their ages ranged from 50 to 92 years; their education levels ranged from 0 to 19 years, and 63% of them had never attended school. We administered the IQCODE to informants and the Cognitive Abilities Screening Instrument (CASI), from which a CASI-estimated score of the MMSE (MMSE-CE) can be obtained, to the subjects. The diagnosis of dementia was made independently by physicians according to the DSM-III-R criteria based on semistructured interview and testing, neurologic examination, and standardized assessments of cerebral vascular disease, Parkinson's disease, and depression. The Chinese IQCODE showed no association with the subjects' education level or gender, low association with their age, and moderately high association with their MMSE-CE score. The area under the receiver operating characteristic curve of the IQCODE was significantly larger than that of the MMSE-CE for the whole group and for the subgroup with 1 to 19 years of education but not for the subgroup with 0 years of education. Nine of the 26 items of the IQCODE could be deleted without appreciable reduction in sensitivity and specificity. The IQCODE (1) can be shortened to 17 items, (2) had good cross-cultural applicability, and (3) was better than the MMSE-CE as a screening tool for dementia in a population with large variation in educational backgrounds.
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PMID:The Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) as a screening tool for dementia for a predominantly illiterate Chinese population. 782 43

The syndrome of gait ignition failure is described in six patients in whom difficulty initiating walking was the major symptom. The gait had elements of parkinsonism with start and turn hesitation, shuffling, and freezing. Unlike parkinsonism, however, the gait was relatively normal once entrained; the posture was upright, and good arm swing, a normal stride length, and no festination were seen. Equilibrium was normal or near normal, and when seated or lying, rhythmic leg movements were generated normally. Facial expression, upper limb mobility, and whole body movements were well-preserved. This gait disorder differed from that seen in Parkinson's disease and the so-called "frontal" or "senile" disorders of gait and gait "apraxia." The causes of this gait syndrome are not clear but it may be due to frontal lobe vascular disease and/or focal degeneration of the frontal lobes.
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PMID:The syndrome of gait ignition failure: a report of six cases. 834 Dec 92

Brain is a logical target of free radical damage, considering the large lipid content of myelin sheaths and the high rate of brain oxidative metabolism. Thus, the hypothesis that free radicals may be involved in the pathogenesis of certain CNS diseases has gained increasing popularity in recent years. In CNS ischemia-reperfusion injury, the role of free radicals appears to be well established, however, involvement of other factors, such as excitatory amino acids and prostaglandins, may also contribute to the production of neuronal necrosis following ischemia. Liberation of free iron appears to play a crucial role in the generation of reactive oxygen species in posttraumatic epilepsy. Although there is no direct evidence to indicate free radical involvement in the pathogenesis of Alzheimer's disease, brain trauma with release of iron, amyloid angiopathy and disturbances in blood-brain barrier function all appear to contribute to the development of ischemic episodes with free radical generation and neuronal degeneration. In Parkinson's disease, the substantia nigra appears to be under oxidative stress as evidenced by the findings of increased lipid peroxidation, reduced GSH levels, high concentration of iron and free radical generation via autocatalytic mechanisms within neuromelanin-containing catecholaminergic neurons. Regardless of the initial insult, a cascade of events involving both reactive oxygen radicals and mitochondrial metabolism is likely to contribute to cell injury.
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PMID:Oxygen, antioxidants and brain dysfunction. 837 80

Cytidine 5'-diphosphocholine, CDP-choline or citicoline, is an essential intermediate in the biosynthetic pathway of the structural phospholipids of cell membranes, especially in that of phosphatidylcholine. Upon oral or parenteral administration, CDP-choline releases its two principle components, cytidine and choline. When administered orally, it is absorbed almost completely, and its bioavailability is approximately the same as when administered intravenously. Once absorbed, the cytidine and choline disperse widely throughout the organism, cross the blood-brain barrier and reach the central nervous system (CNS), where they are incorporated into the phospholipid fraction of the membrane and microsomes. CDP-choline activates the biosynthesis of structural phospholipids in the neuronal membranes, increases cerebral metabolism and acts on the levels of various neurotransmitters. Thus, it has been experimentally proven that CDP-choline increases noradrenaline and dopamine levels in the CNS. Due to these pharmacological activities, CDP-choline has a neuroprotective effect in situations of hypoxia and ischemia, as well as improved learning and memory performance in animal models of brain aging. Furthermore, it has been demonstrated that CDP-choline restores the activity of mitochondrial ATPase and of membranal Na+/K+ ATPase, inhibits the activation of phospholipase A2 and accelerates the reabsorption of cerebral edema in various experimental models. CDP-choline is a safe drug, as toxicological tests have shown; it has no serious effects on the cholinergic system and it is perfectly tolerated. These pharmacological characteristics, combined with CDP-choline's mechanisms of action, suggest that this drug may be suitable for the treatment of cerebral vascular disease, head trauma of varying severity and cognitive disorders of diverse etiology. In studies carried out on the treatment of patients with head trauma, CDP-choline accelerated the recovery from post-traumatic coma and the recuperation of walking ability, achieved a better final functional result and reduced the hospital stay of these patients, in addition to improving the cognitive and memory disturbances which are observed after a head trauma of lesser severity and which constitute the disorder known as postconcussion syndrome. In the treatment of patients with acute cerebral vascular disease of the ischemic type, CDP-choline accelerated the recovery of consciousness and motor deficit, attaining a better final result and facilitating the rehabilitation of these patients. The other important use for CDP-choline is in the treatment of senile cognitive impairment, which is secondary to degenerative diseases (e.g., Alzheimer's disease) and to chronic cerebral vascular disease. In patients with chronic cerebral ischemia, CDP-choline improves scores on cognitive evaluation scales, while in patients with senile dementia of the Alzheimer's type, it slows the disease's evolution. Beneficial neuroendocrine, neuroimmunomodulatory and neurophysiological effects have been described. CDP-choline has also been shown to be effective as co-therapy for Parkinson's disease. No serious side effects have been found in any of the groups of patients treated with CDP-choline, which demonstrates the safety of the treatment.
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PMID:CDP-choline: pharmacological and clinical review. 870 78

In this study, the antigenic expression of CD34, a 110 kDa glycoprotein which is expressed on human haemopoietic progenitor cells and vascular endothelium, has been assessed in a variety of neuropathological conditions, including infectious and demyelinating disease. Using immunoperoxidase staining on paraffin sections, the immunohistochemical results show that CD34 antigen is expressed widely on human CNS endothelium in grey and white matter, in the eye including retina, and in the anterior and posterior lobes of the pituitary. In demyelinating disease CD34 antigen expression was not detected in acute lesions, whereas strong expression was observed in old lesions. CD34 endothelial positivity was observed in areas of gliosis, vasogenic oedema, vascular disease and in Alzheimer's and Parkinson's disease pathology. A general pattern emerged, with CD34 antigen reactivity predominantly negative in areas of inflammation with demyelination but positive in adjacent non-inflamed tissue, irrespective of myelin pathology. We conclude that perivascular inflammation is a key factor in the absence of immunoreactivity of CD34 in the CNS in demyelinating disease.
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PMID:The expression of the endothelial cell antigen CD34 in demyelinating disease. 873 85

It is not known whether an increased incidence of dementia in patients with Parkinson's disease (PD) is due to a higher incidence of Alzheimer's disease (AD) or to "early" Alzheimer-type pathology. To determine whether amyloid beta-peptide (A beta) of AD occurs more frequently in brains of patients with PD, we examined 50 cases and 79 controls by using histoblots for A beta. Twenty-three cases with PD had dementia, including all nine with A beta distributed throughout the entire cerebral cortex; three of these cases had AD. In contrast, five of 17 controls with comparable A beta accumulation were not demented. Neither AD nor A beta deposition was increased in PD, furthermore, there was no statistical correlation between the amount of A beta and the number of Lewy bodies in cerebral cortex. In 14 patients with PD in whom dementia was unrelated to A beta, there was cerebral vascular disease (four), numerous cortical Lewy bodies (three), or hydrocephalus (two); in five further cases, dementia was not well explained by histopathologic changes. Our data found no increase of either AD or "early" Alzheimer-type pathology in cases of PD; however, a synergistic effect between the two pathologies was suggested as contributing to dementia.
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PMID:Amyloid beta-peptide and the dementia of Parkinson's disease. 891 90

L-Dopa is the most effective drug known for the treatment of Parkinson's disease. However, the large doses required to treat this neurodegenerative disorder can significantly affect tissue concentrations of sulfur amino acid metabolites due to peripheral and central O-methylation. These effects include decreases in tissue concentrations of the biochemical methyl donor S-adenosylmethionine (SAM), increases in tissue concentrations of the methylation inhibitor S-adenosylhomocysteine (SAH), and increases in plasma concentrations of homocysteine, recently identified as an independent risk factor for vascular disease. In the present study, the ability of the catechol-O-methyltransferase inhibitor Ro 41-0960 to prevent L-Dopa-induced changes in SAM, SAH, and homocysteine concentrations was determined in rats. Rats were injected intraperitoneally with Ro 41-0960 or vehicle 30 min prior to an intraperitoneal injection of L-Dopa or vehicle. One hour after the second injection, the rats were killed and their brains, livers, spleens, kidneys, and plasma collected. SAM and SAH concentrations were then determined in discrete brain regions and peripheral tissues, and total homocysteine concentrations were determined in plasma. In the rats treated with only L-Dopa, decreased SAM concentrations and increased SAH concentrations were found in all brain regions and peripheral tissues measured, and increased homocysteine concentrations were found in plasma, consistent with previous reports. In rats pretreated with Ro 41-0960, however, these L-Dopa-induced effects on sulfur amino acid metabolite concentrations were attenuated or prevented entirely. It remains to be determined if this sparing effect of Ro 41-0960 on sulfur amino acid metabolites has clinical significance.
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PMID:Effect of L-Dopa and the catechol-O-methyltransferase inhibitor Ro 41-0960 on sulfur amino acid metabolites in rats. 903 74


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