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)

To assess the need for a regional expertise in movement disorders, the numbers of patients, clinic visits, and medication changes for a new movement disorder clinic were recorded. During 3 1/2 years, 355 patients were seen, with 1,329 clinic visits. Idiopathic Parkinson's disease was the most common diagnosis, comprising 36% of the population, followed by dystonia (17%), tremor (12%), parkinsonism (i.e., Parkinson's plus syndromes, drug-induced parkinsonism, etc.) (10%), chorea (10%), Tourette's syndrome (6.5%), and tardive dyskinesia (3.4%). Distribution of follow-up visits was similar, with Parkinson's disease (52%) being most frequent and Tourette's syndrome (3.1%) least frequent. The relative utilization of medical care by each patient group was assessed by determining the number of medication changes and the number of clinic visits per follow-up year. No differences in these measures were found using a one-way analysis of variance. Of the Parkinson's disease patients, 67% had Hoehn and Yahr stages III-IV and 77% of the clinic visits were made by this subgroup. When considered in light of the prevalence of each of the diseases, these data show a need for an expertise in movement disorders for a population base of the size we have served.
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PMID:Profile of patients enrolled in a new movement disorder clinic. 175 52

The classification of dopamine receptors and their neuroanatomical distribution is reviewed, including the newly discovered D3, D4 and D5 subtypes. In vivo imaging techniques and methods for quantification are briefly described and PET and SPECT studies of D2 receptors in schizophrenia, under neuroleptic treatment, in aging, Parkinson's disease, Huntington's disease, tardive dyskinesia and multisystem atrophies are reviewed and compared with our own results. A short description is given of imaging studies of D1 receptors.
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PMID:Dopamine receptor classification, neuroanatomical distribution and in vivo imaging. 177 98

Since the initial observation by Brown (1914) that electrical stimulation applied to the habenular efferent bundle in the chimpanzee evoked a pattern of respiration which closely resembled the act of laughter, the habenular complex has remained a mysterious structure. The anatomy of the habenular complex is well delineated (Jones, 1985) forming a major component of the dorsal diencephalic conduction system. Data derived mainly from animal experimentation over the past decade point to the fact that the habenular complex functions as an important link between the limbic forebrain and the midbrain-extrapyramidal motor system. The elucidation of the functions of the habenular complex may thus significantly increase the current insight into the understanding of the interaction between behavioral and motor functions. Clearly, such information would be of great relevance for further understanding of neuropsychiatric disorders such as schizophrenia, Parkinson's disease, Tardive dyskinesia, and Tourette's syndrome in which behavioral and motor impairments are interfaced. This review summarizes anatomical, functional, and pharmacological aspects of the habenular complex and discusses its potential contribution to the pathophysiology of selected neuropsychiatric and movement disorders.
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PMID:Relevance of the habenular complex to neuropsychiatry: a review and hypothesis. 182 82

Dopamine receptors belong to the family of G protein-coupled receptors. On the basis of the homology between these receptors, three different dopamine receptors (D1, D2, D3) have been cloned. Dopamine receptors are primary targets for drugs used in the treatment of psychomotor disorders such as Parkinson's disease and schizophrenia. In the management of socially withdrawn and treatment-resistant schizophrenics, clozapine is one of the most favoured antipsychotics because it does not cause tardive dyskinesia. Clozapine, however, has dissociation constants for binding to D2 and D3 that are 4 to 30 times the therapeutic free concentration of clozapine in plasma water. This observation suggests the existence of other types of dopamine receptors which are more sensitive to clozapine. Here we report the cloning of a gene that encodes such a receptor (D4). The D4 receptor gene has high homology to the human dopamine D2 and D3 receptor genes. The pharmacological characteristics of this receptor resembles that of the D2 and D3 receptors, but its affinity for clozapine is one order of magnitude higher. Recognition and characterization of this clozapine neuroleptic site may prove useful in the design of new types of drugs.
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PMID:Cloning of the gene for a human dopamine D4 receptor with high affinity for the antipsychotic clozapine. 184 Jun 45

Free radicals are reactive chemical species with an unpaired electron that are produced through a variety of physiologic and pathologic processes. Free radicals have been implicated in a variety of neuropsychiatric conditions, many of which are marked by the gradual development of psychopathologic symptoms and movement disorder. There is evidence that radical-induced damage may be important in Parkinson's disease, tardive dyskinesia, metal intoxication syndromes, and Down's syndrome, and possibly also in schizophrenia, Huntington's disease, and Alzheimer's disease. Although some of this evidence is highly speculative, it may offer an avenue for further understanding and treatment of these conditions.
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PMID:Oxygen radicals and neuropsychiatric illness. Some speculations. 184 28

Oxygen free radicals, any chemical moiety containing an oxygen atom with an unpaired electron in the outer orbital shell, are generated during many normal biochemical reactions in living tissue. The unpaired electron makes these compounds highly reactive and they can initiate disruptive peroxidation reactions with various substrates important to the survival of cells such as proteins, lipids and nucleic acids. A fairly complex defense system has evolved to protect living tissue from free radicals and to minimize the damage they might cause. Neurons are especially vulnerable to free radical attack and impaired defenses or exposure to excess free radicals can lead to neuronal death. Free radicals contribute to neuronal loss in cerebral ischemia and hemorrhage and may be involved in the degeneration of neurons in epilepsy, schizophrenia, tardive dyskinesia, normal aging, Parkinson's Disease and Alzheimer's Disease. The development of drugs that limit or prevent the attack of free radicals on neurons would be an important advance in the treatment of these conditions.
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PMID:Oxygen free radicals and brain dysfunction. 134 20

MIF-1, a synthetic tripeptide with MSH-release inhibitory properties, has been reported to improve symptoms of Parkinson's disease, attenuate levodopa-related dyskinesias and diminish the dyskinetic movements of Tardive dyskinesia. More recently, MIF-1 has been reported partially to protect against the nigro-striatal dopamine depleting effects of MPTP in mice, raising the possibility that it may exert protective effects against the development of Parkinson's disease. There is evidence to suggest that MIF-1 increases nigro-striatal dopaminergic activity, but its ability to improve symptoms in patients with Parkinson's disease, levodopa-related dyskinesias and Tardive dyskinesia cannot be explained solely on the basis of the drug's effect on striatal dopaminergic neurons. MIF-1 has been reported to potentiate the melanocyte-lightening effect of melatonin in rats and its effects in patients with Parkinson's disease and Tardive dyskinesia are associated with marked mood elevation. It is, therefore, possible that the effects of MIF-1 in movement disorders are associated with increased melatonin secretion. Thus, hypothalamic MIF may modulate nigro-striatal dopaminergic functions in part via pineal melatonin. Such an interaction represents a novel mechanism by which hypothalamic peptides act to modulate the expression of movement disorders.
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PMID:MIF-induced augmentation of melatonin functions: possible relevance to mechanisms of action of MIF-1 in movement disorders. 197 68

Alterations in the density of dopamine receptor subtypes and behaviors mediated by the D1-selective agonist SKF-38393 were examined in rats treated chronically with reserpine, SKF-38393 or the combination of these drugs. Animals received either vehicle or reserpine (1 mg/kg s.c.) on days 1 to 28 and, in addition, half of each of these groups were treated with vehicle and half were treated with SKF-38393 (5-10 mg/kg s.c.) on days 15 to 29. Quantitative autoradiographic measurement of D1 receptors labeled with [3H]SCH-23390 and D2 receptors labeled with [3H]spiroperidol revealed that chronic administration of reserpine increased the density of both receptor subtypes in the nucleus accumbens and caudate-putamen, but not in the substantia nigra. Chronic administration of SKF-38393 alone did not alter D1 receptor density in any of these regions. However, chronic administration of the agonist in reserpinized animals decreased D1 receptor density in the nucleus accumbens, but not in the caudate-putamen or substantia nigra, demonstrating that this partial agonist can selectively down-regulate D1 receptors when endogenous dopaminergic tone is removed. The chronic drug treatments also altered behavioral responses. Chronic administration of SKF-38393 alone produced sensitization of the oral dyskinesia response elicited by a challenge injection of the agonist, but no significant change in the grooming response. Acute administration of SKF-38393 in rats treated with reserpine for 14 days produced stereotypy which was not altered after chronic administration of the agonist. Surprisingly, chronic administration of reserpine alone produced a spontaneous oral dyskinesia, which was blocked dose-dependently by the D2-selective antagonist spiroperidol. These findings are discussed in terms of their relevance to Parkinson's disease and tardive dyskinesia.
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PMID:Behavioral and neurochemical effects of chronic administration of reserpine and SKF-38393 in rats. 203 24

Videotapes of patients with Huntington's chorea, tardive dyskinesia (TD), and L-DOPA-induced chorea in Parkinson's disease were taken while the patients were seated with their legs dangling. The videotapes were scored in a blinded fashion for suppressibility of dyskinesias. Most patients with TD or L-DOPA-induced chorea substantially suppressed their involuntary movements, whereas most patients with Huntington's chorea did not. There was a small overlap between the TD and Huntington's chorea groups and suppressibility therefore could not absolutely distinguish between them. Suppressibility testing may nonetheless be a valuable clinical tool since a good, excellent, or complete suppressibility rating was highly suggestive of TD but not Huntington's chorea. TD and L-DOPA-induced chorea may be more pathophysiologically similar to each other than either is to Huntington's chorea.
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PMID:A blinded study of the suppressibility of involuntary movements in Huntington's chorea, tardive dyskinesia, and L-dopa-induced chorea. 214 44

Alterations in blink rate have been reported in several neuropsychiatric disorders presumed to result from abnormal central dopaminergic functions. Increased blink rate in schizophrenia, Tardive dyskinesia, Tourette's syndrome and Meige's disease are associated with enhanced dopaminergic functions. Parkinson's disease is associated with reduced dopaminergic functions and decreased blink rate. Thus, blink rate may reflect striatal and mesolimbic dopaminergic activity. Since acute light exposure suppresses melatonin production and darkness stimulates melatonin secretion, blinking may serve to regulate light-dark exposure to the pineal gland and thus to 'fine tune' melatonin production. As there is evidence to suggest that melatonin inhibits the release of dopamine in the striatum and limbic system, increased blink rate may serve to reduce light exposure, increase melatonin secretion and attenuate dopaminergic functions. Conversely, decreased blinking (as is observed in patients with Parkinson's disease) could reflect a compensatory mechanism to increase light exposure, reduce melatonin production and ultimately increase dopamine functions. This model is novel in that for the first time it suggests a functional link among blink rate, melatonin secretion and striatal dopaminergic functions in movement disorders.
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PMID:The significance of eye blink rate in parkinsonism: a hypothesis. 226 15


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