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 Kraepelinian subtypes, developed early in the century, recognize the heterogeneity of schizophrenia but do not reliably predict differences in response to classical neuroleptics. The newer distinction of positive and negative syndromes in schizophrenia carry promise as an approach to identifying meaningful clinical and neurobiological dimensions. The present review summarizes the supportive evidence from a series of investigations using the Positive and Negative Syndrome Scale (PANSS), and a hypothesis on the pathophysiology of negative and positive symptoms is advanced. Our data suggest that: (a) positive and negative syndromes in schizophrenia represent stable, independent dimensions and not co-exclusive subtypes; (b) both are unrelated to the progression of illness; (c) they are differentially related to fundamental aspects of schizophrenia, including premorbid adjustment, cognitive development, family psychiatric history, the cognitive and neuropsychiatric profiles, dopaminergic functions, drug response, and subsequent course; (d) together with depression and excitement, they comprise the fundamental symptomatic components of schizophrenia, which, in their interaction, can account for the specific Kraepelinian subtypes. We have proposed that negative symptoms represent the core pathology in schizophrenia and may be understood as a variant of parkinsonism, hence characterized by dopaminergic deficiency and increased cholinergic activity. This view is supported by the striking overlap with Parkinsonism in regard to clinical features, neurochemistry, pharmacology, neuropathology, and neuroradiology. Positive symptoms are thought to reflect increased dopaminergic activity, which may arise as a compensatory adaptive mechanism to overcome the progressive dopamine loss in the maturing brain. The early onset of schizophrenia by comparison to Parkinson's disease may explain why schizophrenia entails more pronounced positive symptoms, development deficits, and cognitive, social, and emotional impairments. We describe evidence that pineal calcification, which may reflect disturbance of melatonin functions, appears to be a nongenetic factor in schizophrenia associated with perinatal injury. This may in part underlie the negative syndrome and its response to antipsychotic compounds with serotonergic (5-HT) antagonism.
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PMID:Experimental models of schizophrenia. 193 75

The cerebrospinal fluid (CSF) is a specific ultrafiltrate of plasma, which surrounds the brain and spinal cord. The study of its proteins and their alteration may yield useful information on several neurological diseases. By using various electrophoretic separation techniques, several CSF proteins have been identified derived from plasma or from brain. Different one-dimensional methods, such as agarose gel electrophoresis and isoelectric focusing, are of similar value in identifying the non-specific oligoclonal bands, which are mainly helpful in the diagnosis of multiple sclerosis and other inflammatory diseases. Isoelectric focusing has a greater resolution than other one-dimensional methods, and it yields additional data about disease-associated proteins occurring in Alzheimer's disease, Huntington's chorea and amyotrophic lateral sclerosis. Silver-stained two-dimensional gels provide more information about the complex protein composition of CSF, particularly about proteins produced in the brain, such as apolipoprotein E and neuron-specific enolase. For the detection of oligoclonal antibodies, the investigation of protein changes revealed by Parkinson's disease, schizophrenia and Creutzfeldt-Jakob disease, and the analysis of CSF immune complexes, two-dimensional electrophoresis has a greater sensitivity.
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PMID:Analysis of cerebrospinal fluid proteins by electrophoresis. 193 90

Thirty years ago, dopamine was identified as an essential neurotransmittor. Since then, it has been the most written about CNS molecule. Considerable evidence implicates disturbances of brain dopamine function in the pathophysiology of several psychiatric and neurologic disorders, especially schizophrenia and Parkinson's disease. In the last decade, there have been important advances in the understanding of the diversity of CNS dopamine neurons and the chemical basis of this diversity, which relies upon molecular physiology of D1 and D2 receptors. Heterogeneity is remarkable at different levels, anatomical, biochemical, morphological or functional; besides, region specific interactions with other neurotransmittors and sometimes colocalisation of dopamine with cholecystokinin and/or neurotensin suggest the integration of dopamine neurons in functional subunits.
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PMID:[The mesencephalic dopaminergic system. Implications for neuroleptic treatment]. 197 42

Receptors for dopamine have been classified into two functional types, D1 and D2. They belong to the family of receptors acting through G (or guanine nucleotide-binding) proteins. D2 receptors inhibit adenylyl cyclase, but D1 receptors stimulate adenylyl cyclase and activate cyclic AMP-dependent protein kinases. Dopamine D1 and D2 receptors are targets of drug therapy in many psychomotor disorders, including Parkinson's disease and schizophrenia, and may also have a role in drug addiction and alcoholism. D1 receptors regulate neuron growth and differentiation, influence behaviour and modify dopamine D2 receptor-mediated events. We report here the cloning of the D1 receptor gene, which resides on an intronless region on the long arm of chromosome 5, near two other members of the G-linked receptor family. The expressed protein, encoded by 446 amino acids, binds drugs with affinities identical to the native human D1 receptor. The presence of a D1 receptor gene restriction fragment length polymorphism will be helpful for future disease linkage studies.
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PMID:Human dopamine D1 receptor encoded by an intronless gene on chromosome 5. 197 40

1. The tetradecapeptide somatostatin (SS) has a widespread, uneven distribution within several organs including the central nervous system (CNS), with particularly high concentration in the hypothalamus. 2. The SS-related peptides (SS28, SS28(1-12), SS28(15-28)) are originated from the precursor pre-prosomatostatin. 3. SS is suggested to be involved in a large number of CNS functions, locomotion, sedation, excitation, catatonia, body temperature, feeding, nociception, paradoxical sleep, self-stimulation, seizure, learning and memory. 4. SS influences central neurochemical processes. 5. It is possible that SS is related to various neurological and psychiatric illnesses, like Huntington's disease, multiple sclerosis, Parkinson's disease, epilepsy, eating disorders, Alzheimer's disease, schizophrenia and major depressive illness.
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PMID:Preclinical and clinical studies with somatostatin related to the central nervous system. 197 75

Positron-emission tomography (PET), a noninvasive analytical method, made possible the detection of regional alterations in the central nervous system, thus demonstrating "in vivo" the presence of biochemical alterations and the organization of cerebral function in the pathological states. The study of glucose cerebral metabolism velocity, performed recently with the aid of PET, reveals that in the patients with thymic disorders the values recorded for the bipolar syndromes differ from those recorded the for unipolar ones. At the same time, the direct measurement of the activity of the neuroanatomic structures involved in schizophrenia and their response to neuroleptics was possible. This technique and the F-fluoro-desixiglucose method were also applied to the patients with Alzheimer's disease, multi-infarct dementia, Huntington's disease. Wilson's disease and Parkinson's disease. Suggestive alterations of glucose metabolism velocity were noticed and the neuroanatomic structures involved in the pathological manifestations could be specified.
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PMID:[The use of positron-emission tomography in psychiatry]. 198 25

We have determined the erythrocyte membrane uptake of the monoamine precursors L-tyrosine (L-TYR) and L-tryptophane (L-TRYP) in 72 patients with schizophrenia: 21 without neuroleptic treatment and not depressed, 15 with neuroleptic treatment and depressed, 33 without neuroleptic treatment, 27 depressed, compared to: 59 control subjects, and 54 depressed patients. We found that the ratio of L-TYR facilitated membrane diffusion to that of L-TRYP is: decreased when the patients are depressed, increased when they are untreated. When untreated patients receive neuroleptics and are depressed, the ratio tends to equal that of depressed patients'. The meaning of these anomalies is analysed, using our up-to-date knowledge of the erythrocytes's role in uptaking and dispatching the human body amino-acids, and of the role of these uptakes in regulating the functional monoamine balance. We postulate that in depressions, Parkinson's disease and schizophrenia, a change of membrane fluidity occurs, being decreased in depressions and Parkinsons's disease, and increased in schizophrenia.
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PMID:[Erythrocyte membrane transports of monoamine precursor amino acids in schizophrenia]. 204 99

The transplantation (at an experimental level) of embryonic and fetal nerve tissue from different parts of the encephalon yields new possibilities for its use in humans in the future. The recent clinical application in the treatment of schizophrenia and Parkinson's disease is just the beginning to the long road toward cerebral reconstruction. The authors believe that this technique can also be used in the treatment of infantile cerebral palsy.
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PMID:[Infantile cerebral palsy. The current status and future prospects of treatment]. 205 23

The psychotic features of schizophrenia and the motor problems of Parkinson's disease, respectively, allow striking contrasts to be made between the two disorders. However, it has recently become apparent that the two groups of patients share problems of mentation that are best explained by some dysfunction of the prefrontal cortical areas of the brain. These commonalities are addressed in terms of neurobiological fact and psychological theory, providing possible insight into the neuropsychology of schizophrenia and its dichotomous nature. In particular, the putative role of abnormal frontostriatal interactions in the two disease states is emphasized.
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PMID:Frontal lobe dysfunction in schizophrenia and Parkinson's disease--a meeting point for neurology, psychology and psychiatry: discussion paper. 206 3

The diverse physiological actions of dopamine are mediated by its interaction with two basic types of G protein-coupled receptor, D1 and D2, which stimulate and inhibit, respectively, the enzyme adenylyl cyclase. Alterations in the number or activity of these receptors may be a contributory factor in diseases such as Parkinson's disease and schizophrenia. Here we describe the isolation and characterization of the gene encoding a human D1 dopamine receptor. The coding region of this gene is intronless, unlike the gene encoding the D2 dopamine receptor. The D1 receptor gene encodes a protein of 446 amino acids having a predicted relative molecular mass of 49,300 and a transmembrane topology similar to that of other G protein-coupled receptors. Transient or stable expression of the cloned gene in host cells established specific ligand binding and functional activity characteristic of a D1 dopamine receptor coupled to stimulation of adenylyl cyclase. Northern blot analysis and in situ hybridization revealed that the messenger RNA for this receptor is most abundant in caudate, nucleus accumbens and olfactory tubercle, with little or no mRNA detectable in substantia nigra, liver, kidney, or heart. Several observations from this work in conjunction with results from other studies are consistent with the idea that other D1 dopamine receptor subtypes may exist.
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PMID:Molecular cloning and expression of the gene for a human D1 dopamine receptor. 214 34


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