Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A clinical trial was conducted in 22 SLE patients with central nervous system (CNS) disorder in which the efficacy of pulse methylprednisolone suleptanate at the dose of 400 mg or 800 mg (as methylprednisolone) was assessed. The symptoms of CNS disorder disappeared within 40 days after pulse therapy in all of the 16 patients with organic brain syndrome (OBS). No improvement in the symptoms took place in any but one of the five patients who had cerebrovascular disorder. One SLE patient with depression showed improvement 55 days after pulse therapy. In the patients with OBS who had not received pulse therapy until 28 days or more after onset of CNS disorder, the symptoms disappeared in 20 days or more in both 400 mg and 800 mg dose groups. On the other hand, five of the six patients given the dose of 800 mg within 10 days of occurrence of the disease experienced a complete relief of the symptoms in 10 days after pulse therapy. However, at least 13 days were required for complete relief in all the four patients of the 400 mg group. The adverse reactions reported consisted of hyperlipemia, diabetes mellitus, and infections such as thrush or herpes zoster. The above results suggest that methylprednisolone pulse therapy is useful in the treatment of CNS disorder associated with SLE, particularly in patients with OBS who are given the dose of 800 mg early after onset of the disease.
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PMID:[Methylprednisolone pulse therapy for SLE patients with CNS disorder]. 797 24

The neuropsychiatric manifestations of HIV disease include neurobiologic and psychobiologic phenomena. The former consist of primary CNS complications caused directly by HIV, and include cognitive disorders (mild neurocognitive disorder and HIV-associated dementia) and other CNS diseases such as myelopathy and the demyelinating neuropathies; and secondary disorders (principally deliria) occasioned by opportunistic infections, neoplasms, cerebrovascular events, and the effects of metabolic derangements and medications. The latter (psychobiologic) phenomena reflect efforts to cope with various nodal, or transition points, in HIV disease; such points of transition include time of serostatus determination, adaptation to asymptomatic seropositivity, response to early medical symptomatology, and later transition to frank AIDS. Anxiety symptoms and various efforts to cope with anxiety (e.g., denial, anger, withdrawal, hypochondriacal preoccupation) all can punctuate these transition points. Additionally, there may be reactivation of long-standing psychopathology (e.g., depression) in seropositive individuals who tend to belong to a group that has an elevated prevalence of pre-infection psychiatric disorder. These interacting neurobiologic and psychobiologic phenomena pose challenges to the psychiatrist who must develop a good understanding of the medical aspects of HIV infection, as well as the neuropsychiatry of AIDS. In this way psychiatric physicians can play an important role in early identification of neuropsychiatric complications, assist the medical team to anticipate emotional and behavioral disturbances, and develop treatment plans that maximize our ability to help those with HIV infection achieve the best possible quality of life.
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PMID:Natural history of neuropsychiatric manifestations of HIV disease. 819 Jun 64

The routine diagnosis of tuberculosis and other mycobacterial diseases based on organism identification was completed during a period of one year in 730 patients, with serological IgG, IgM and IgA determination of antibodies against antigen 60 from M. bovis , strain BCG. The analysis was performed on 10 groups of patients consisting of 1) inflammatory diseases of the respiratory tract, 2) pericarditis, myocarditis, lymphadenitis and CNS diseases, 3) chronic non-inflammatory diseases of kidneys, liver and pancreas, 4) non-inflammatory diseases of the heart, sarcoidosis and pneumoconiosis, 5) tumor, 6) healthy people with TB contact, 7) inactive TB, 8) culture-positive pulmonary and extra-pulmonary TB, 9) culture-negative TB and extra-pulmonary TB, and 10) potentially pathogenic mycobacteria. The specificity of the test (100% negative cases in Group 6, composed of healthy people) is estimated at about 90%, in accordance with determinations made in other laboratories. In non-tuberculous patients, the specificity varied according to the analysed groups. Group 1 was largely unspecific for IgM (76% positives) but the specificity was acceptable for IgG (6.2% positives ) and IgA (7.4% positives). Group 2 was similar to Group 1. Group 3 was associated with positive IgA titers. Group 4 was only exceptiony seropositive and Group 5 was positive mainly for IgA (11. 4%) associated with lower respiratory tract ailments. This unspecific seropositivity was attributed to inapparent infections by PPM whose colonisation was favored by the particular disease of the patients. The sensitivity of serological measurements applied to the diagnosis of TB patients and PPM patients was similar, regardless if the disease was pulmonary or non-pulmonary, regardless if cultures were positive or not and, in our hands, was low (positivity for IgA about 30 %, for IgM about 10% and for IgG about 30%). This poor sensitivity observed with people presenting for treatment is attributed to an immune depression occuring mainly in elderly patients. The remarkable sensitivity of the serological instrument applied to culture-negative pulmonary and non-pulmonary TB cases as well as PPM cases makes the test a good adjuvant in cases of suspicion of TB. The assessment of the serological status of people under chemotherapy is worth the analysis, a high IgG level being associated with immunocompetence while the absence of IgG antibodies and/or the presence of IgA antibodies denotes an immunologically misdirected response potentially opening the way to chronic infections.
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PMID:Serological IgG, IgM and IgA diagnosis and prognosis of mycobacterial diseases in routine practice. 936 Sep 40

Recent advances in nutritional and biochemical research have documented inositol as an important dietary and cellular constituent. The processes involved in inositol metabolism and its derivatives in the tissues of mammals have been characterized in vivo as well as at the enzymatic level. Biochemical functions defined for phosphatidylinositol in biological membranes include the regulation of cellular responses to external stimuli and/or nerve transmission as well as the mediation of enzyme activity through interactions with various specific proteins. Altered production of inositol has been documented in patients with diabetes mellitus, chronic renal failure, galactosemia, and multiple sclerosis. Inositol has been reported to be effective in treating central nervous system disorders such as depression, Alzheimer's disease, panic disorder, and obsessive-compulsive disorder. It has documented benefit for use in pediatric respiratory depression syndrome. In addition, recent studies have evaluated its usefulness as an analgesic. Inositol has been studied extensively as potential treatment to alleviate some negative effects associated with lithium therapy. The use of inositol in pregnant women remains controversial. Although its benefit in preventing neural tube defects in embryonic mice is documented, the risk of inducing uterine contractions limits its usefulness in pregnancy.
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PMID:Inositol--clinical applications for exogenous use. 985 68

Histamine H3 receptor ligands have been proposed to be of potential therapeutic interest for the treatment of different central nervous system disorders; however, the psychopharmacological properties of these drugs have not been studied extensively. In this work, we investigated the possible involvement of histamine H3 receptor function in experimental models of anxiety (elevated plus-maze) and depression (forced swimming test). Male Sprague-Dawley rats were treated i.p. with the histamine H3 receptor agonist R-alpha-methylhistamine (10 mg/kg) or the histamine H3 receptor antagonist thioperamide (0.2, 2 and 10 mg/kg) and 30 min afterwards the time spent in the open arms of an elevated plus-maze was registered for 5 min. The immobility time of male OF1 mice in the forced swimming test was recorded for 6 min, 1 h after the i.p. administration of R-alpha-methylhistamine (10 and 20 mg/kg), thioperamide (0.2, 2, 10 and 20 mg/kg) or another histamine H3 receptor antagonist, clobenpropit (5 mg/kg). The locomotor activity of mice was checked in parallel by means of an activity meter. Both saline controls and active drug controls were used in all the paradigms. Neither thioperamide nor R-alpha-methylhistamine significantly changed animal behaviour in the elevated plus-maze. R-alpha-methylhistamine and the higher dose of thioperamide assayed (20 mg/kg) were also inactive in the forced swimming test. By contrast, thioperamide (0.2-10 mg/kg) dose-dependently decreased immobility, the effect being significant at 10 mg/kg (33% reduction of immobility); clobenpropit produced an effect qualitatively similar (24% reduction of immobility). None of these histamine H3 receptor antagonists affected locomotor activity. These preliminary results suggest that the histamine H3 receptor blockade could be devoid of anxiolytic potential but have antidepressant effects. Besides, the stimulation of these receptors does not seem to be followed by changes in the behavioural parameters studied.
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PMID:Effects of histamine H3 receptor ligands in experimental models of anxiety and depression. 1010 75

HIV-1 infection can be associated with neuropsychological (NP) deficits ranging from subtle to severe. The purpose of this study was to evaluate the functional, or "real-world" impact of HIV-associated NP impairment in a group of 267 HIV-infected participants. All participants received comprehensive NP, neuromedical, and standardized functional evaluations that included laboratory measures of shopping, cooking, financial management, medication management and vocational abilities. Compared to NP-normal participants, those with NP impairment performed significantly worse on all laboratory measures of everyday functioning. Multivariate analyses revealed that the NP ability domains of Abstraction/Executive Function, Learning, Attention/Working Memory and Verbal abilities most strongly and consistently predicted failures on the functional battery. Both NP impairment and impairment on the functional battery were significantly associated with subjective experiences of cognitive difficulties, as well as unemployment and increased dependence in activities of daily living; multivariate prediction models that also considered depressed mood and biological measures of disease progression revealed that impairment on the functional battery and depression were the only unique predictors of all three indicators of "real-world" functioning. The current results add to growing evidence concerning the clinical significance of HIV-associated NP impairment. Objective, laboratory based functional measures, such as those used here, may compliment NP testing in future studies directed at understanding the impact on life quality of central nervous system disorders and their treatments. Finally, there is a need for additional research investigating the apparently independent effect of depression on level of everyday functioning in HIV infected persons.
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PMID:The impact of HIV-associated neuropsychological impairment on everyday functioning. 1514 90

Advances in a multitude of disciplines support an emerging role for cytochrome P450 enzymes and their metabolic substrates and end-products in the pathogenesis and treatment of central nervous system disorders, including acute cerebrovascular injury, such as stroke, chronic neurodegenerative disease, such as Alzheimer's and Parkinson's disease, as well as epilepsy, multiple sclerosis and psychiatric disorders, including anxiety and depression. The neural tissue contains its own unique set of P450 genes that are regulated in a manner that is distinct from their molecular regulation in peripheral tissue. Furthermore, brain P450s catalyze the formation of important brain signaling molecules, such as neurosteroids and eicosanoids, and metabolize substrates as diverse as vitamins A and D, cholesterol, bile acids, as well as centrally acting drugs, anesthetics and environmental neurotoxins. These unique characteristics allow this family of proteins and their metabolites to perform such vital functions in brain as neurotrophic support, neuroprotection, control of cerebral blood flow, temperature control, neuropeptide release, maintenance of brain cholesterol homoeostasis, elimination of retinoids from CNS, regulation of neurotransmitter levels and other functions important in brain physiology, development and disease.
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PMID:Cytochrome P450 in neurological disease. 1518 Apr 92

In the last decade, a large number of studies using Delta9-tetrahydrocannabinol (THC), the main active principle derivative of the marijuana plant, or cannabinoid synthetic derivatives have substantially contributed to advance the understanding of the pharmacology and neurobiological mechanisms produced by cannabinoid receptor activation. Cannabis has been historically used to relieve some of the symptoms associated with central nervous system disorders. Nowadays, there are anecdotal evidences for the use of cannabis in many patients suffering from multiple sclerosis or chronic pain. Following the historical reports of the use of cannabis for medicinal purposes, recent research has highlighted the potential of cannabinoids to treat a wide variety of clinical disorders. Some of these disorders that are being investigated are pain, motor dysfunctions or psychiatric illness. On the other hand, cannabis abuse has been related to several psychiatric disorders such as dependence, anxiety, depression, cognitive impairment, and psychosis. Considering that cannabis or cannabinoid pharmaceutical preparations may no longer be exclusively recreational drugs but may also present potential therapeutic uses, it has become of great interest to analyze the neurobiological and behavioral consequences of their administration. This review attempts to link current understanding of the basic neurobiology of the endocannabinoid system to novel opportunities for therapeutic intervention and its effects on the central nervous system.
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PMID:Role of endocannabinoid system in mental diseases. 1532 60

Some piperidine-based nocaine/modafinil hybrid ligands have been designed, synthesized, and found to display an improved potency at all three monoamine transporters and particularly for DAT and/or NET. Some highly active and selective monoamine transporter inhibitors with low nanomolar to subnanomolar potency were identified. Ligands of this type may find important applications as positron emission tomography imaging tools and in the treatment of central nervous system disorders such as depression and sleep apnea.
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PMID:Piperidine-based nocaine/modafinil hybrid ligands as highly potent monoamine transporter inhibitors: efficient drug discovery by rational lead hybridization. 1553 37

Descending monoaminergic systems modulate spinal cord function, yet spinal dopaminergic actions are poorly understood. Using the in vitro lumbar cord, we studied the effects of dopamine and D2-like receptor ligands on spinal reflexes in wild-type (WT) and D3-receptor knock-out mice (D3KO). Low dopamine levels (1 microM) decreased the monosynaptic "stretch" reflex (MSR) amplitude in WT animals and increased it in D3KO animals. Higher dopamine concentrations (10-100 microM) decreased MSR amplitudes in both groups, but always more strongly in WT. Like low dopamine, the D3 receptor agonists pergolide and PD 128907 reduced MSR amplitude in WT but not D3KO mice. Conversely, D3 receptor antagonists (GR 103691 and nafadotride) increased the MSR in WT but not in D3KO mice. In comparison, D2-preferring agonists bromocriptine and quinpirole depressed the MSR in both groups. Low dopamine (1-5 microM) also depressed longer-latency (presumably polysynaptic) reflexes in WT but facilitated responses in D3KO mice. Additionally, in some experiments (e.g., during 10 microM dopamine or pergolide in WT), polysynaptic reflexes were facilitated in parallel to MSR depression, demonstrating differential modulatory control of these reflex circuits. Thus, low dopamine activates D3 receptors to limit reflex excitability. Moreover, in D3 ligand-insensitive mice, excitatory actions are unmasked, functionally converting the modulatory action of dopamine from depression to facilitation. Restless legs syndrome (RLS) is a CNS disorder involving abnormal limb sensations. Because RLS symptoms peak at night when dopamine levels are lowest, are relieved by D3 agonists, and likely involve increased reflex excitability, the D3KO mouse putatively explains how impaired D3 activity could contribute to this sleep disorder.
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PMID:Conversion of the modulatory actions of dopamine on spinal reflexes from depression to facilitation in D3 receptor knock-out mice. 1560 40


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