Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The recent development of genetic databases and biobanks in a number of countries reflects scientist's beliefs in the future health benefits to be derived from genetic research. The NEPSYBANK is a national program of the Hungarian Clinical Neurogenetic Society with comprehensive participation of the Neurology and Psychiatry Departments of Medical Universities and the National Institute of Psychiatry and Neurology. The NEPSYBANK forms a part of the national biobank project (www.biobank.hu). The goal is to establish nationwide collaboration and common biobanking standards on quality, access, and protection of integrity in the field of neurology and psychiatry. Biological materials and databases are already collected in stroke, epilepsy, multiple sclerosis, motoneuron diseases, dementia, movement disorders, schizophrenia, and alcohol addiction. In peripheral neuropathies, neuropathic pain syndromes, muscle diseases, migraine, myasthenia gravis, depression, panic disease, anxiety, autism, and software development is in progress. The resources have been expanded by continued prospective collection of samples and data and important bottlenecks in sample purification, sample retrieval, in protection of the integrity of the research participants, as well as in guaranteeing the security and confidentiality of the participant's information have been harmonized. The development of uniform consent management, comprehensive sample overview and quality standards for health care-related biobanking may provide a unique opportunity for Hungary in molecular clinically oriented research. The program is a diseased-based research biobank with comprehensive collection of phenotypic and environmental information as well as biobanking of DNA, RNA or buffy coat, plasma, and erythrocytes stored at -80 degrees C. The biobank has a neuropathological part as well: storing conventional pathology and biopsy specimens. The analytical and informational demands being created by biobanking requires a "connectivity of community" that has not traditionally been present in the life sciences. As you put more resources into something, your silos tend to become taller, and we need to avoid this. The life science and healthcare community should be ignored working in individual "silos."
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PMID:Establishing a neurological-psychiatric biobank: banking, informatics, ethics. 1744 54

Valproic acid is increasingly used in the treatment of epilepsy, and also prescribed for bipolar affective disorders, schizoaffective disorders, schizophrenia and migraine prophylaxis. Valproic acid intoxication with suicide attempt is a relatively common clinical problem that can result in coma, respiratory depression, pancytopenia, hemodynamic instability and death. The drug's relatively low molecular weight, small volume of distribution and saturable protein-binding render it potentially amenable to exracorporeal removal (hemodialysis, hemoperfusion or hemofiltration ), but published experience is scarce. We describe a case report involving valproic acid intoxication with ingestion of ethanol, who was successfully treated with charcoal hemoperfusion. With this treatment the half-life of valproic acid was reduced with rapid lowering of valproic acid levels and clinical improvement. Based on our experience in this patient and a review of previously reported cases, charcoal hemoperfusion should be considered for serious valproic acid intoxication because free as well as bound drug fractions are eliminated via this technique.
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PMID:[Hemoperfusion in the treatment of acute valproic acid intoxication]. 1772 57

Serotonin (5-HT) receptors are part of the G protein-coupled and ligand-gated ion channel families. 5-HT exerts its diverse actions by binding to cell surface receptors which can be classified into seven distinct families (5-HT1 to 5-HT7) according to their structural diversity and mode of action. Some of the 5-HT families are comprised of multiple receptors which share similar structural and mechanistic properties but display very different operational profiles. Evidence continues to mount in support of the important roles of the 5-HT receptors in various neuropsychiatric disorders such as anxiety, depression, schizophrenia, migraine and drug addiction. The 5-HT receptors may also play an important role in obesity, aggression, sexual behaviour and cardiovascular disorders. A number of selective/non-selective 5-HT agonist and antagonist ligands (drugs) have been developed to challenge many of these disease states.
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PMID:5-hydroxytryptamine (5-HT) receptor ligands. 1789 4

Once considered little more than the glue that holds neurons in place, astrocytes are now becoming appreciated for the key roles they play in central nervous system functions. They supply neurons and oligodendrocytes with substrates for energy metabolism, control extracellular water and electrolyte homeostasis, regulate neurotransmitter release, modulate immune responses, produce trophic factors, and control synapse formation. Astrocytes express receptors for many neurotransmitters, peptides, hormones and cytokines, and show excitability based on intracellular Ca2+ variations. Evidence is mounting that alterations in astrocyte functionality play a crucial role in the pathogenesis of disorders with diverse properties, including migraine, epilepsy, leukodystrophies, inflammatory demyelinating diseases, infections, brain edema and metabolic disorders, metal intoxications, neurodegenerative disorders, and schizophrenia. Targeting astrocyte dysfunction may lead to new therapeutic strategies for these disorders.
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PMID:Dysfunctional astrocytes as key players in the pathogenesis of central nervous system disorders. 1793 36

The short chain fatty acid valproic acid (VPA, 2-propylpetanoic acid) is approved for the treatment of epilepsia, bipolar disorders and migraine and clinically used for schizophrenia. In 1999, the first clinical anti-cancer trial using VPA was initiated. Currently, VPA is examined in numerous clinical trials for different leukaemias and solid tumour entities. In addition to clinical assessment, the experimental examination of VPA as anti-cancer drug is ongoing and many questions remain unanswered. Although other mechanisms may also contribute to VPA-induced anti-cancer effects, inhibition of histone deacetylases appears to play a central role. This review focuses on recent developments regarding the anti-cancer activity of VPA.
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PMID:Valproic acid as anti-cancer drug. 1804 92

Presynaptic receptors for dopamine, histamine and serotonin that are located on dopaminergic, histaminergic and sertonergic axon terminals, respectively, function as autoreceptors. Presynaptic receptors also occur as heteroreceptors on other axon terminals. Auto- and heteroreceptors mainly affect Ca(2+) -dependent exocytosis from the receptor-bearing nerve ending. Some additionally subserve other presynaptic functions.Presynaptic dopamine, histamine and serotonin receptors are involved in various (patho)physiological conditions. Examples are the following:Dopamine autoreceptors play a role in Parkinson's disease, schizophrenia and drug addiction. Dopamine heteroreceptors affecting the release of acetylcholine and of amino acid neurotransmitters in the basal ganglia are also relevant for Parkinson's disease. Peripheral dopamine heteroreceptors on postganglionic sympathetic terminals influence heart rate and vascular resistance through modulation of noradrenaline release. Blockade of histamine autoreceptors increases histamine synthesis and release and may support higher CNS functions such as arousal, cognition and learning. Peripheral histamine heteroreceptors on C fiber and on postganglionic sympathetic fiber terminals diminish neuropeptide and noradrenaline release, respectively. Both inhibititory effects are beneficial in myocardial ischemia. The inhibition of neuropeptide release also explains the antimigraine effects of some agonists of presynaptic histamine receptors. Upregulation of presynaptic serotonin autoreceptors is probably involved in the pathogenesis of major depression. Correspondingly, antidepressant treatments can be linked with a reduced density of 5-HT autoreceptors. 5-HT Heteroreceptor activation diminishes acetylcholine and GABA release and may therefore increase anxiety. In the periphery, presynaptic 5-HT heteroreceptor agonists shorten migraine attacks by inhibition of the release of neuropeptides from trigeminal afferents, apart from their constrictive action on meningeal vessels.
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PMID:Presynaptic receptors for dopamine, histamine, and serotonin. 1806 18

Antiepileptic drugs (AEDs) are used extensively to treat multiple non-epilepsy disorders, both in neurology and psychiatry. This article provides a review of the clinical efficacy of AEDs in non-epilepsy disorders based on recently published preclinical and clinical studies, and attempts to relate this efficacy to the mechanism of action of AEDs and pathophysiological processes associated with the disorders. Some newer indications for AEDs have been established, while others are under investigation. The disorders where AEDs have been demonstrated to be of clinical importance include neurological disorders, such as essential tremor, neuropathic pain and migraine, and psychiatric disorders, including anxiety, schizophrenia and bipolar disorder. Many of the AEDs have various targets of action in the synapse and have several proposed relevant mechanisms of action in epilepsy and in other disorders. Pathophysiological processes disturb neuronal excitability by modulating ion channels, receptors and intracellular signalling pathways, and these are targets for the pharmacological action of various AEDs. Attention is focused on the glutamatergic and GABAergic synapses. In psychiatric conditions such as schizophrenia and bipolar disorder, AEDs such as valproate, carbamazepine and lamotrigine appear to have clear roles based on their effect on intracellular pathways. On the other hand, some AEDs, e.g. topiramate, have efficacy for nonpsychiatric disorders including migraine, possibly by enhancing GABAergic and reducing glutamatergic neurotransmission. AEDs that seem to enhance GABAergic neurotransmission, e.g. tiagabine, valproate, gabapentin and possibly levetiracetam, may have a role in treating neurological disorders such as essential tremor, or anxiety disorders. AEDs with effects on voltage-gated sodium or calcium channels may be advantageous in treating neuropathic pain, e.g. gabapentin, pregabalin, carbamazepine, oxcarbazepine, lamotrigine and valproate. Co-morbid conditions associated with epilepsy, such as mood disorders and migraine, may often respond to treatment with AEDs. Other possible disorders where AEDs may be of clinical importance include cancer, HIV infection, drug and alcohol abuse, and also in neuroprotection. A future challenge is to evaluate the second-generation AEDs in non-epilepsy disorders and to design clinical trials to study their effects in such disorders in paediatric patients. Differentiation between the main mechanisms of action of the AEDs needs more consideration in drug selection for tailored treatment of the various non-epilepsy disorders.
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PMID:Antiepileptic drugs in non-epilepsy disorders: relations between mechanisms of action and clinical efficacy. 1807 13

Potassium (K+) channels are the most heterogeneous and widely distributed class of ion channels. K(+) channels are dynamic pore-forming transmembrane proteins known to play important roles in all cell types underlying both normal and pathophysiological functions. Essential for such diverse physiological processes as nerve impulse propagation, muscle contraction, cellular activation and the secretion of biologically active molecules, various K(+) channels are recognized as potential therapeutic targets in the treatment of multiple sclerosis, Alzheimer's disease, Parkinson's disease, epilepsy, stroke, brain tumors, brain/spinal cord ischemia, pain and schizophrenia, migraine, as well as cardiac arrhythmias, pulmonary hypertension, diabetes, cervical cancer, urological diseases and sepsis. In addition to their importance as therapeutic targets, certain K(+) channels are gaining attention for their beneficial roles in anesthesia, neuroprotection and cardioprotection. The K(+) channel gene families (subdividing into multiple subfamilies) include voltage-gated (K(v): K(v)1-K(v)12 or KCNA-KCND, KCNF-KCNH, KCNQ, KCNS), calcium-activated (K(Ca): K(Ca)1-K(Ca)5 or KCNM-KCNN), inwardly rectifying (K(ir): K(ir)1-K(ir)7 or KCNJ) and background/leak or tandem 2-pore (K(2P): K(2P)1-K(2P)7, K(2P)9-K(2P)10, K(2P)12-K(2P)13, K(2P)15-K(2P)18 or KCNK) K(+) channels. Worldwide, the pharmaceutical industry is actively developing better strategies for targeting ion channels, in general, and K(+) channels, in particular, already generating over $6 billion in sales per annum from drugs designed to block or modulate ion channel function. This review provides an overview of recent patents on emerging K(+) channel blockers and activators (openers) with potential for development as new and improved nervous system therapeutic agents.
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PMID:Potassium channel blockers and openers as CNS neurologic therapeutic agents. 1822 Dec 32

Mining of the human genome has revealed approximately 7000 novel proteins, which could serve as potential targets for the development of novel therapeutics. Of these, approximately 2000 are predicted to be G-protein coupled receptors. Within this group of proteins, a family of 18 mammalian receptors has recently been identified that appear to exhibit selectivity toward the so-called trace amines. The trace amines are a family of endogenous compounds with strong structural similarity to classical monoamine neurotransmitters, consisting primarily of 2-phenylethylamine, m- and p-tyramine, tryptamine, m- and p-octopamine and the synephrines. The endogenous levels of these compounds are at least two orders of magnitude below those of neurotransmitters such as dopamine, noradrenaline and 5-HT. The effects of these low physiological concentrations have been difficult to demonstrate but it has been suggested that they may serve to maintain the neuronal activity of monoamine neurotransmitters within defined physiological limits. Such an effect of trace amines would make them ideal candidates for the development of novel therapeutics for a wide range of human disorders. Although the demonstration of a trace amine family of receptors has seen a resurgence of interest in these endogenous compounds, with recent articles reviewing trace amine pharmacological and physiological responses, the potential clinical utility of the trace amine receptors has not been specifically addressed. Historically, trace amines have been implicated in a diverse array of human pathologies ranging from schizophrenia to affective disorders to migraine. Recent studies have strengthened some of this historical data by linking trace amine receptor polymorphisms and mutations to distinct clinical conditions. The aim of the current article is to review the previous studies linking trace amines to human pathology in the context of the recently discovered trace amine receptors and evidence of the existence of trace amine receptor polymorphisms and mutations associated with such disorders. In addition, recent evidence linking trace amines to the development of drug dependence will be discussed.
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PMID:The potential of trace amines and their receptors for treating neurological and psychiatric diseases. 1847 83

We review a growing body of medical and physiological evidence indicating that yawning may be a thermoregulatory mechanism, providing compensatory cooling when other provisions fail to operate favorably. Conditions such as multiple sclerosis, migraine headaches, epilepsy, stress and anxiety, and schizophrenia have all be linked to thermoregulatory dysfunction and are often associated with instances of atypical yawning. Excessive yawning appears to be symptomatic of conditions that increase brain and/or core temperature, such as central nervous system damage, sleep deprivation and specific serotonin reuptake inhibitors. Yawning is also associated with drowsiness, and subjective ratings of sleepiness are correlated with increases in body temperature. This view of yawning has widespread application for the basic physiological understanding of thermoregulation as well as for the improved diagnosis and treatment of diseases associated with abnormal thermoregulation.
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PMID:Yawning and thermoregulation. 1855 Jan 30


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