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)

The age-adjusted prevalence of PSP as measured in central New Jersey is 1.5 cases per million population, about 1% of that of Parkinson's disease. It incidence is 3-4 new cases per million population per year, similar to that of such better-known illnesses as myasthenia gravis, the hereditary ataxias as a group and Tourette syndrome. Median actuarially adjusted survival after symptom onset is 5.9-6.9 years. PSP appears to favor no geographical, racial, ethnic or occupational group, though there is anecdotal evidence for hydrocarbon exposure as a candidate etiologic factor. No familial cases of typical PSP have been proven. The one formal case-control study failed to implicate any particular causal agent and the rural predilection of PD appears to be absent in PSP. Better diagnostic methods, more multi-center organization, additional case-control studies and new etiologic hypotheses are needed in the epidemiological investigation of PSP.
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PMID:The epidemiology of PSP. 796 91

The carrier molecule that transports dopamine (DA) across the synaptic membrane is known as the dopamine transporter (DAT). Depending on the ionic conditions, DAT may function as a mediator of both the inward directed DA transport known as the "reuptake" and the outward directed DA transport known as the "release." The functional significance of DAT is in the regulation of DA neurotransmission by terminating the action of DA in the synapse via reuptake. With use of DAT binding as a presynaptic marker to measure altered DA innervation, abnormalities of the DAT binding have been demonstrated in idiopathic Parkinson's disease, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity, and progressive supranuclear palsy. Moreover, the identification of DAT as the neuronal element that mediates the addictive properties of cocaine highlights its significance in cocaine addiction. Cocaine binding in the brain is heterogeneous, and there is an uneven distribution of the high- and low-affinity binding sites across the anatomical regions. Regional differences in ligand binding are observed by using both [3H]cocaine and the diphenyl-substituted piperazine derivatives known as the "GBR series" of ligands. The identification of compounds that inhibit the binding of medications for cocaine abuse. Furthermore, clarification of the various binding domains that may be relevant to transporter function in human neuropsychiatric disorders may lead to the development of new medications for schizophrenia, Tourette's disease, and drug addiction.
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PMID:Molecular, functional and biochemical characteristics of the dopamine transporter: regional differences and clinical relevance. 814 55

The blink reflex and its recovery curve were studied in 12 patients with neurologic and psychiatric disorders, i.e., juvenile Parkinson's disease (case 1), Gilles de la Tourette's syndrome (case 2), anorexia nervosa (case 3), mild developmental delay (cases 4 and 5), a meningomyelocele with winking spasms (case 6), Parkinson's disease (cases 7-10) and OPCA (cases 11 and 12). The cases were divided into 4 groups on the basis of the results, (1) hyperexcitability of facial motoneurons only (case 6), (2) hyperexcitability of facial motoneurons and brainstem interneurons (case 1 and 2), (3) hyperexcitability of brainstem interneurons only (cases 4, 5 and 7-12) and (4) hypoexcitability of both sides (case 3). Therefore, as to the excitability an abnormal pattern of blink reflexes could be a neurophysiologic marker of some neurologic and psychiatric disorders.
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PMID:The excitability of blink reflexes in patients with neurologic and psychiatric disorders. 818 76

The dopamine transporter (DAT) is the carrier protein that transports dopamine across the presynaptic membrane. The DAT terminates the action of dopamine (DA) in the synapse via reuptake and thus regulates DA neurotransmission. The transporter has been studied by direct binding techniques using a variety of ligands which are inhibitors of DA transport. DAT binding, both in vivo (positron emission tomography) and in vitro (post mortem) may serve as a presynaptic marker to measure altered DA innervation in several neuropsychiatric diseases such as idiopathic Parkinson's disease, Tourette's disease, schizophrenia or cocaine addiction. In Parkinson's disease, a reduction in the density of binding sites could be due either to a degeneration of the terminal dopaminergic projections or to a compensatory readjustment in the level of dopamine synaptic transmission. This dopaminergic cell specific marker could also aid in attempts to elucidate the rate at which dopaminergic cells are lost in this disease. MPTP (a neurotoxin which induces a parkinsonian-like syndrome after conversion in MPP+) uses DAT to enter the neuron and exert its toxic effect which may be prevented by pretreatment with DA uptake blockers. In cocaine abuse, DAT mediates the addictive properties of cocaine. Cocaine binding sites on the carrier may be distinct from DA binding sites allowing the development of medication sparing the DA function but impairing the cocaine effects. In schizophrenia, functional DA uptake was reported to be increased in the striatum in post mortem brains, whereas the kinetic parameters of the uptake sites were unchanged using different transporter labeling ligands. Thus, this marker does not provide any evidence for the dopaminergic hypothesis, but an impairment of the DAT itself could possibly be involved in the etiology of schizophrenia. However, the possible interaction of drugs such as L-Dopa or neuroleptic treatment with transporter binding may be taken into account in the results analysis. Finally, the DAT gene is also an important candidate gene for psychiatric diseases such as schizophrenia or cocaine abuse.
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PMID:[The dopamine transporter: characterization and physiopathologic implications]. 867 69

Nicotine maintains tobacco addiction and has therapeutic utility to aid smoking cessation and possibly to treat other medical diseases. Nicotine acts on nicotinic cholinergic receptors, which demonstrate diversity in subunit structure, function, and distribution within the nervous system, presumably mediating the complex actions of nicotine described in tobacco users. The effects of nicotine in people are influenced by the rate and route of dosing and by the development of tolerance. The metabolism of nicotine is now well characterized in humans. A few individuals with deficient C-oxidation of nicotine, unusually slow metabolism of nicotine, and little generation of cotinine have been described. Nicotine affects most organ systems in the body, although its contribution to smoking-related disease is still unclear. Nicotine as a medication is currently available as a gum, a transdermal delivery device, and a nasal spray, all of which are used for smoking cessation. Nicotine is also being investigated for therapy of ulcerative colitis, Alzheimer's disease, Parkinson's disease, Tourette's syndrome, sleep apnea, and attention deficit disorder.
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PMID:Pharmacology of nicotine: addiction and therapeutics. 872 3

Patients with hyperkinetic basal-ganglia disorders (Huntington's disease, HD; and Tourette's syndrome, TS) have difficulty with spatially incongruent stimulus-response configurations, the Simon effect, and with inhibiting inappropriate responses in a conditionality paradigm. However Parkinson's disease (PD) patients with hypokinetic basal-ganglia disorder show normal (for their age) conditionality and congruency effects, probably because the task is extremely sensitive to aging and PD patients are typically older than HD and TS individuals. Overall, HD patients were by far the most affected, reflecting the likely greater involvement of the caudate (with its predominantly cognitive role) than the putamen; the latter structure, with a predominantly motor involvement, is the more affected in PD.
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PMID:Simon effect and attention in Parkinson's disease: a comparison with Huntington's disease and Tourette's syndrome. 878 Sep 62

The proceedings of the inaugural scientific meeting of the Society for Research on Nicotine and Tobacco (SRNT) are summarized. The primary objective of the meeting was to foster the exchange of information on the effects of nicotine and tobacco use, as well as factors which influence their use, drawing from biological, behavioral and social sciences. Much of this research can be viewed as a tale of "two" drugs--nicotine as a key to an important public health problem, and nicotine as a classical tool of physiological and pharmacological research. A historical overview of research on "both" drugs is provided first. Public policy alternatives for reducing the prevalence of tobacco use have been derived in part from basic and clinical research results and are briefly outlined. Evidence for genetic determinants on nicotine use and effects is presented using data from twin studies and from molecular genetic research with humans and animals. Consistent with this research, there is evidence of individual differences in pharmacokinetics and effects of nicotine, which could account for differences in smoking behavior and nicotine dependence. Finally, recent developments in the therapeutic uses of nicotine and novel nicotinic agonists with schizophrenia, Alzheimer's disease, Parkinson's disease, Tourette's syndrome and ulcerative colitis are presented. Overall, the research presented at the meeting demonstrated the vast diversity of areas of study involving nicotine and tobacco, as well as the rich opportunities for cross-communication among researchers from different disciplines.
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PMID:Society for Research on Nicotine and Tobacco. 882 21

Huntington's disease (HD) and Tourette's syndrome (TS) are two basal ganglia (BG) disorders, associated not simply with hyperkinetic movements but also with attentional impairments. The purpose of this experiment was to evaluate the attention deficits reported in HD and TS via the use of a vibrotactile choice reaction time (CRT) procedure involving biased probabilities of event occurrence. We attempted to ascertain whether HD and TS patients are impaired in their ability to shift their attention to an unexpected location, or when they have to hold attention to an expected location. The results demonstrate that HD patients, as compared to controls, experience difficulties in shifting their attention from expected to unexpected spatial locations; this effect was exacerbated with the adoption of a crossed arm configuration. On the other hand, TS patients' performance, although slower overall, was not qualitatively greatly different from that of the controls. We had previously found, with a similar paradigm, that Parkinson's disease patients instead manifest problems in holding or maintaining attention to an expected locus. We conclude that HD patients experience considerable difficulties in allocating attentional resources between expected and unexpected event occurrences. Perhaps due to pervasive subcortical damage and dysfunction in the circuits linking the frontal lobes with the BG. In TS, a similar if milder functional rather than structural deficit may be reflected in a pattern of responses which resembles a weaker version of the HD response pattern.
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PMID:The effect of Huntington's disease and Gilles de la Tourette's syndrome on the ability to hold and shift attention. 882 31

This article reviews the results of clinical studies with Deprenyl in various neurologic and psychiatric disorders except Parkinson's disease. Promising results could be observed both in narcolepsy in a dose of at least 20 mg/day in three different trials and in one study of Tourette's syndrome including attention hyperactivity disorders using an average dosis of 8.1 mg/ day. Controversial results were reported for Alzheimer's disease. On the one hand significant improvement of cognitive functions was found by various authors. On the other hand in a more recent study no effect on the progression of the disease could be observed. For depression a higher dosage of deprenyl between 30 to 60 mg/day appears to be necessary for effective treatment. No positive results were found in amyotrophic lateral sclerosis and in tardive dyskinesias.
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PMID:The clinical potential of Deprenyl in neurologic and psychiatric disorders. 898 64

Nicotine has various effects in the CNS, especially in dopaminergic and cholinergic systems, relevant in pathophysiology of neuropsychiatric movement disorders. Nicotine acutely reduce the symptomatology in Parkinson's disease. In neuroleptic-induced Parkinsonism (NIP) acute nicotine application induces positive changes of symptomatology. Chronic application, however, leads to a greater likelihood of NIP. The results concerning tardive dyskinesia are not consistent, but nicotine tends to exercise a positive influence on basic mechanisms. In the Gilles-de-la-Tourette syndrome nicotine reduces the severity and frequency of the tics given in combination with haloperidol.
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PMID:[Nicotine in neuropsychiatric movement disorders]. 899 74


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