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

The aim of the study was to evaluate the use of imaging in the development of neuropharmacological drugs. All New Drug Applications (NDAs) approved from 1995 through 2004 in the Division of Neuropharmacological Drug Products at the Food and Drug Administration were surveyed for imaging studies. Imaging literature was also reviewed with respect to antipsychotics and antidepressants. One hundred and six NDAs (35 new molecular entities (NMEs)) were approved; 15 of these NDAs (10 NMEs) had imaging studies. The primary imaging modality was positron emission tomography. Imaging was primarily conducted for drugs used in schizophrenia, depression, multiple sclerosis, and migraine. The majority evaluated receptor occupancy or proof of concept. Examples (including literature) are discussed as pertinent to dosage, efficacy, safety, or further development of a drug or class of drugs. Imaging contributes to optimal clinical development of central nervous system (CNS)-active drugs. Opportunities are available for its broader use, contributing to improved understanding of the clinical pharmacology of CNS-active drugs.
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PMID:The use of imaging in the early development of neuropharmacological drugs: a survey of approved NDAs. 1856 70

Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health and disease. Damage to mitochondria is now understood to play a role in the pathogenesis of a wide range of seemingly unrelated disorders such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis. Medications have now emerged as a major cause of mitochondrial damage, which may explain many adverse effects. All classes of psychotropic drugs have been documented to damage mitochondria, as have stain medications, analgesics such as acetaminophen, and many others. While targeted nutrient therapies using antioxidants or their precursors (e. g., N-acetylcysteine) hold promise for improving mitochondrial function, there are large gaps in our knowledge. The most rational approach is to understand the mechanisms underlying mitochondrial damage for specific medications and attempt to counteract their deleterious effects with nutritional therapies. This article reviews our basic understanding of how mitochondria function and how medications damage mitochondria to create their occasionally fatal adverse effects.
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PMID:Medication-induced mitochondrial damage and disease. 1862 87

The serotonin (5-HT) 5-HT(7) receptors are expressed in both the central nervous system and in peripheral tissues. Receptor distribution studies and pharmacological studies have established that 5-HT(7) receptors play an important role in the control of circadian rhythms and thermoregulation. Selective 5-HT(7) receptor ligands have potential therapeutic applications for the treatment of pain and migraine, schizophrenia, anxiety, cognitive disturbances and inflammation. We have cloned two novel C-terminal splice variants of the 5-HT(7) receptor from mouse brain. These two new splice variants have almost identical sequences as the rat 5-HT(7(b)) and 5-HT(7(c)) splice variants and so were given the same name. Ligand binding assays ([(3)H]5-CT), membrane localization and functional studies in transiently transfected cells indicated that all three splice variants are well expressed on the membrane and no major differences in their respective pharmacology and their ability to activate adenylyl cyclase were observed. This is in analogy with previous reports comparing either the rat or the human variants.
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PMID:Cloning, genomic organization and functionality of 5-HT(7) receptor splice variants from mouse brain. 1879 7

Professor TIAN's experiences on acupuncture treatment of various difficult diseases with different acupuncture methods based on syndrome differentiation of different patients, for example, para-acupuncture for treatment of migraine, triple puncture at Dazhui (GV 14) for recurrent depression, lifting and thrusting point Shexiaxue for treatment of aphasia, electroacupuncture at Shuigou (GV 26) and Baihui (GV 20) for treatment of schizophrenia, etc. are introduced.
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PMID:[Professor TIAN Cong-huo's experience on clinical acupuncture]. 1897 34

The XXVI Collegium Internationale Neuro-Psychopharmacologicum (CINP) Congress, commemorating its 50th anniversary, was held in Munich, Germany, from July 13 to 17, 2008, at the Internationales Congress Center. Co-incidentally, this year Munich is also celebrating its 850th birthday and venerating various events. Keeping its tradition, the CINP Congress addressed the main issues related to mental depression, schizophrenia and anxiety disorders. The various symposia addressed topics such as immunology in psychiatry, status of conventional and atypical antipsychotics, risks and benefits in long-term use of selective serotonin reuptake inhibitors, interrelating the role of various neurotransmitters, particularly, dopamine and glutamate in psychiatry and animals models employed in central nervous system disorders. The congress also addressed educational issues such as state-of-the-art treatment of various psychiatric disorders. This was in line with the current observations of the World Health Organization (WHO) database, according to which approximately 1 billion people worldwide are battling neurological disorders ranging from migraines to epilepsy and dementia. The economic burden of both treatment and loss of social workforce is huge even though several remedies are available for the management of these disorders. Therefore, the CINP rightly addressed the issues of discovering new targets and therapeutic options in the management of neuropsychiatric disorders. The conference also brought together scientists involved in basic or clinical research. The present article summarizes the outcome of the deliberations.
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PMID:New therapeutic promises in the treatment of depression and schizophrenia. 1922 39

After 40 years of investigation, steady-state visually evoked potentials (SSVEPs) have been shown to be useful for many paradigms in cognitive (visual attention, binocular rivalry, working memory, and brain rhythms) and clinical neuroscience (aging, neurodegenerative disorders, schizophrenia, ophthalmic pathologies, migraine, autism, depression, anxiety, stress, and epilepsy). Recently, in engineering, SSVEPs found a novel application for SSVEP-driven brain-computer interface (BCI) systems. Although some SSVEP properties are well documented, many questions are still hotly debated. We provide an overview of recent SSVEP studies in neuroscience (using implanted and scalp EEG, fMRI, or PET), with the perspective of modern theories about the visual pathway. We investigate the steady-state evoked activity, its properties, and the mechanisms behind SSVEP generation. Next, we describe the SSVEP-BCI paradigm and review recently developed SSVEP-based BCI systems. Lastly, we outline future research directions related to basic and applied aspects of SSVEPs.
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PMID:Steady-state visually evoked potentials: focus on essential paradigms and future perspectives. 1996 32

Cerebral imaging and olfactory disorders: a review. Olfactory disorders are often misjudged and rarely given due clinical consideration. Nevertheless, they occur in a wide range of neurological disorders, and their evaluation can help in diagnosis. Whereas psychophysical tests have been used to evaluate olfactory dysfunction in numerous diseases, functional brain imaging using olfactory stimuli is an emergent technique and few studies have been published to date. After a reminder of cerebral imaging and analysis techniques and a rapid description of our actual knowledge of olfactory processes in healthy subjects, the current review focuses on cerebral imaging studies performed on patients with neurological disorders and presenting olfactory dysfunction. Neurological disorders such as Alzheimer's disease, Parkinson's disease, epilepsy, migraine, multiple chemical sensitivity and schizophrenia are examined.
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PMID:Cerebral imaging and olfactory disorders: a review. 2008 6

Caffeine causes most of its biological effects via antagonizing all types of adenosine receptors (ARs): A1, A2A, A3, and A2B and, as does adenosine, exerts effects on neurons and glial cells of all brain areas. In consequence, caffeine, when acting as an AR antagonist, is doing the opposite of activation of adenosine receptors due to removal of endogenous adenosinergic tonus. Besides AR antagonism, xanthines, including caffeine, have other biological actions: they inhibit phosphodiesterases (PDEs) (e.g., PDE1, PDE4, PDE5), promote calcium release from intracellular stores, and interfere with GABA-A receptors. Caffeine, through antagonism of ARs, affects brain functions such as sleep, cognition, learning, and memory, and modifies brain dysfunctions and diseases: Alzheimer's disease, Parkinson's disease, Huntington's disease, Epilepsy, Pain/Migraine, Depression, Schizophrenia. In conclusion, targeting approaches that involve ARs will enhance the possibilities to correct brain dysfunctions, via the universally consumed substance that is caffeine.
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PMID:Caffeine and adenosine. 2016 66

Reporting bias represents a major problem in the assessment of health care interventions. Several prominent cases have been described in the literature, for example, in the reporting of trials of antidepressants, Class I anti-arrhythmic drugs, and selective COX-2 inhibitors. The aim of this narrative review is to gain an overview of reporting bias in the medical literature, focussing on publication bias and selective outcome reporting. We explore whether these types of bias have been shown in areas beyond the well-known cases noted above, in order to gain an impression of how widespread the problem is. For this purpose, we screened relevant articles on reporting bias that had previously been obtained by the German Institute for Quality and Efficiency in Health Care in the context of its health technology assessment reports and other research work, together with the reference lists of these articles.We identified reporting bias in 40 indications comprising around 50 different pharmacological, surgical (e.g. vacuum-assisted closure therapy), diagnostic (e.g. ultrasound), and preventive (e.g. cancer vaccines) interventions. Regarding pharmacological interventions, cases of reporting bias were, for example, identified in the treatment of the following conditions: depression, bipolar disorder, schizophrenia, anxiety disorder, attention-deficit hyperactivity disorder, Alzheimer's disease, pain, migraine, cardiovascular disease, gastric ulcers, irritable bowel syndrome, urinary incontinence, atopic dermatitis, diabetes mellitus type 2, hypercholesterolaemia, thyroid disorders, menopausal symptoms, various types of cancer (e.g. ovarian cancer and melanoma), various types of infections (e.g. HIV, influenza and Hepatitis B), and acute trauma. Many cases involved the withholding of study data by manufacturers and regulatory agencies or the active attempt by manufacturers to suppress publication. The ascertained effects of reporting bias included the overestimation of efficacy and the underestimation of safety risks of interventions.In conclusion, reporting bias is a widespread phenomenon in the medical literature. Mandatory prospective registration of trials and public access to study data via results databases need to be introduced on a worldwide scale. This will allow for an independent review of research data, help fulfil ethical obligations towards patients, and ensure a basis for fully-informed decision making in the health care system.
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PMID:Reporting bias in medical research - a narrative review. 2038 11

Although the presence of prostaglandin PGF(2?) has been demonstrated in the central nervous system in the mid sixties, it has taken a rather long time to pinpoint a role of certain metabolites of arachidonic acid in the regulation of neural activity. The modern family of bioactive compounds known as "prostanoids" or "eicosanoids" includes the classical end-products of the cyclooxygenase pathway (prostaglandins, prostacyclin and thromboxane), as well as the molecules formed after the activation of 5- and/or 15-lipoxygenases (leucotrienes and lipoxines), 12-lipoxygenase (hepoxilins) or of epoxygenase (epoxides). Although the brain levels of arachidonic acid-the precursor generating prostaglandins from the series 2-are very low, a plethora of stimuli appears to trigger its release from membrane phospholipids mainly by activation of phospholipase A(2) or subordinately phospholipase C; furthermore, its reesterification can also be subtly regulated by endogenous metabolic processes. Numerous prostanoids have now been detected in the nervous system, namely in neurons, astrocytes, cerebrospinal fluid and cerebral vascular endothelium. Efforts have been oriented at the elucidation of the roles of prostanoids in some physiological conditions (for example sleep regulation) or pathological situations (fever, migraine, epilepsy, schizophrenia). Moreover, several investigators have examined the localization of neuronal membrane receptors for prostanoids and searched for the mechanisms of signal transduction or the identity of second messengers. Those embody cyclic nucleotides (cAMP and cGMP) and calcium. There is also compelling evidence for a modulation by prostanoids of the release of noradrenaline, serotonin and vasoactive intestinal peptide (VIP) as well as of several hormones of the hypothalamic-hypophyseal tract. In addition, neurotransmitters can influence prostanoid synthesis; this has been demonstrated in particular for noradrenaline and more recently for acetylcholine. Prostanoids can also amplify neurotransmitter-mediated signals. Thus, ?(1)-adrenergic agonists, H(1)-histaminergic agonists as well as adenosine potentiate cAMP formation elicited by the VIP, through a concomitant generation of prostaglandins mediated by a direct coupling with phospholipase A(2). Baclofen (a GABA(B)-receptor agonist) exerts a similar potentiation mediated in part by the increased activity of 5-lipoxygenase. Furthermore, eicosanoids generated by 12-lipoxygenase are involved in the histamine- or FMRFamide-induced hyperpolarization (opening of K(+) channels) that has been demonstrated in identified sensory neurons of Aplysia. Finally, the stimulation of N- methyl - d - aspartate receptors (a subclass of glutamate receptors) leads to a release of arachidonic acid as well as of 11- and 12-hydroxyeicosatetraenoic acids in cultured striatal neurons. Arachidonic acid and a large number of its classical or recently discovered metabolites therefore display various effects in the central nervous system, both at the level of integrated processes and of the fine synaptic circuitry, where they can act as intracellular or extracellular local messengers triggering new cascades of short term or long term cellular events.
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PMID:Prostanoids and their role in cell-cell interactions in the central nervous system. 2050 6


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