Our in vitro observations showed that memantine was able to prevent the proneurotoxic effects of rtPA in cultured cortical neurons. Although memantine did not alter the fibrinolytic activity of rtPA, our in vivo observations revealed that it blunted the noxious effects of delayed thrombolysis on lesion volumes and neurological deficits after ischemic stroke. In addition, memantine rescued rtPA-induced decrease in survival rate after intracerebral hemorrhage.
To determine the factors associated with receiving specific treatment (cholinesterase inhibitors or/and memantine) for Alzheimer disease (AD) in elderly patients.
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Data were extracted on study characteristics and outcomes, including adverse events. Effect sizes were calculated and data were combined when appropriate.
Although there is no known cure for essential tremor or Parkinson's disease (PD), medical treatment can often significantly reduce or eliminate functional disability. Mild essential tremor does not require treatment, and early treatment does not arrest or slow the natural progression in symptoms. When essential tremor interferes with daily activities, medical treatment options include beta blockers, anticonvulsants, benzodiazepines, and carbonic anhydrase inhibitors. Because of the great variability in the presentation of PD, no single approach is appropriate for all patients. Levodopa is the mainstay of pharmacologic therapy for PD, although other agents are indicated for monotherapy or in combination with levodopa. These include traditional and newer dopamine agonists, amantadine, anticholinergics, selegiline, and an emerging class of agents called COMT inhibitors.
Amantadine, a drug known to inhibit influenza A viral matrix (M2) protein function, was reported to be an effective treatment in some patients with chronic hepatitis C virus (HCV) infection. Sequence comparison shows no homology between M2 and any of the HCV proteins. The effects of amantadine and a related analogue, rimantadine, on viral protease, helicase, ATPase, RNA-dependent RNA polymerase, and HCV internal ribosomal entry site (IRES) translation were tested by established in vitro biochemical assays. No inhibition (>15%) of HCV protease, helicase, ATPase, and polymerase was observed with concentrations up to 400 microgram/mL. IRES-specific inhibition was not observed at clinically relevant concentrations, but both cap and IRES reporter genes were suppressed at higher levels, suggesting nonspecific translation inhibition. In conclusion, amantadine and rimantadine have no direct and specific inhibitory effects against HCV protease, helicase, ATPase, polymerase, and IRES in vitro.
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Randomised controlled trials (RCTs) or quasi-RCTs comparing amantadine and/or rimantadine with no intervention, placebo, other antivirals or different doses or schedules of amantadine or rimantadine in children and the elderly with influenza A.
CYP2D6 polymorphism, though not significant, might partially be involved in the plasma concentration of AD drug.
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Current perspectives on the clinical use of NMDA receptor antagonists infer repeated administration schedules for the management of different pathological states. The development of tolerance and cross-tolerance between different NMDA receptor antagonists may be an important factor contributing to the clinical efficacy of these drugs. The present study aimed to characterize the development of tolerance and cross-tolerance to the ability of various site-selective NMDA receptor antagonists to produce a decrement of operant responding (multiple extinction 9 s fixed-interval 1-s schedule of water reinforcement). Acute administration of D-CPPen (SDZ EAA 494; 1-5.6 mg/kg), dizocilpine (MK-801; 0.03-0.3 mg/kg), memantine (0.3-17 mg/kg), ACEA-1021 (10-56 mg/kg), and eliprodil (1-30 mg/kg) differentially affected operant responding. Both increases and decreases in response rates and accuracy of responding were observed. Repeated preexposure to D-CPPen (5.6 mg/kg, once a day for 7 days) attenuated a behavioral disruption produced by an acute challenge with D-CPPen or ACEA-1021, but potentiated the effects of dizocilpine, memantine, and eliprodil. Based on the present results, one can suggest that the repeated administration of a competitive NMDA receptor antagonist differentially affects the functional activity of various sites on NMDA receptor complex.
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The role of currently available drugs for Alzheimer's disease (AD) has been controversial, with some national formularies restricting their use, and health economists questioning whether the small clinical effects are economically worthwhile.
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Pretreatment HCV p7 was directly sequenced in 157 consecutive patients with chronic HCV genotype 1b infection who had been treated with amantadine/placebo plus pegylated interferon (PEG-IFN)-α2a/ribavirin within a multicentre clinical trial. Triple therapy was preceded by 2 weeks of amantadine/placebo monotherapy. In nine patients, clonal sequencing was performed at baseline and after 2 weeks of amantadine/placebo monotherapy.
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The obtained results show that DTG, the sigma1/sigma2 receptor agonist, exerts a synergistic effect with memantine, an uncompetitive NMDA receptor antagonist, in the forced swimming test in rats, and that progesterone and BD 1047, the sigma1 receptor antagonists, counteract this effect. The results suggest that the sigma1 receptor subtype may contribute to the behavioral response induced by combined administration of DTG and memantine in Porsolt's test in rats.
Plasma dopamine-beta-hydroxylase was studied in 96 subjects, 33 of them controls and 63 of them patients (Parkinson's disease, chronic chorea, torsion dystonia, postural tremor and epilepsy). Only the epileptics showed a significant decrease in the average level of dopamine-beta-hydroxylase activity in comparison with the controls. During the cold test, DBH did not vary except in one case. On the other hand, during epileptic attacks, DBH activity underwent considerable fluctuations. Therefore, except in special pathological conditions, such as epileptic attacks, measurement of plasma or serum DBH activity is of limited value for neurological pathology and is not a good indication of the activity of the sympathetic nervous system.
We enrolled 124 patients with chronic hepatitis C genotype 1. Sixty-three received conventional therapy and 61 patients had triple therapy with amantadine. SVR at week 72 was achieved in 25 patients (39.7%) vs. 26 patients (42.6%) in the double and triple regimen, respectively (p=0.561). After multivariate analysis, advanced fibrosis, obesity, and low pretreatment ALT levels were associated with non-response in both groups (p=0.0234, p=0.0012, p=0.0249, respectively). APRI values delimited an area under the ROC curve (AUROC) of 0.724 and Forns index with AUROC of 0.733. There was no difference between both indices in predicting significant fibrosis (Knodell index: F3-F4).
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To investigate the efficacy and acceptability of dopamine agonists alone or in combination with any psychosocial intervention for the treatment of cocaine abuse and dependence
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Genetic changes in influenza surface and internal genes can alter viral fitness and virulence. Mutation trend analysis and antiviral drug susceptibility profiling of A(H1N1)pdm09 viruses is essential for risk assessment of emergent strains and disease management.
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The study was designed to have 225 HCV nonresponder patients, but at an interim analysis the response rate difference between groups was lower than expected and the enrollment was stopped when 75 patients had been randomized to receive interferon-alpha2a (group A, n = 26), interferon-alpha2a plus 15 mg/kg per day of ribavirin (group B, n = 24), or interferon-alpha2a plus ribavirin plus 200 mg/day of amantadine hydrochloride (group C, n = 25). Treatment duration was 48 weeks. The dose of interferon was 6 MU/day for 4 weeks followed by 3 MU/day for the remaining 44 weeks.
The post-hoc analyses reported here evaluate the specific effects of memantine treatment on ADAS-cog single-items or SIB subscales for patients with moderate to severe AD.
We conducted a single center, double-blind, placebo controlled pilot trial of memantine, titrated to 20 mg/day, in PD subjects. Inclusion criteria were intentionally broad and included both fluctuating and non-fluctuating patients. After baseline assessments, subjects (N = 40) were randomized to drug and placebo groups. They received a battery of traditional and non-motor assessments. After a safety call (2 weeks after baseline) they returned for identical assessments at week 8. An 8-week open label extension was started if desired.
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To systematically review the evidence from randomised and quasi-randomised controlled trials for the effect of any pharmacological or non-pharmacological treatment for PPS compared to placebo, usual care or no treatment.
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A 10-member committee including movement disorder specialists and general neurologists evaluated the available evidence based on a structured literature review including MEDLINE, EMBASE, and Ovid databases from 1965 through June 2004.
A retrospective cohort study.
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NMDA receptors play a role in the aetiology of depression with non-competitive NMDA receptor antagonists such as amantadine showing synergy with conventional antidepressants. To advance a neurochemical rational for these findings, we have studied the effects of administration of amantadine and budipine with the antidepressants reboxetine (REB), paroxetine (PAROX) and clomipramine (CLOM) on extracellular DA in rats using microdialysis. Acutely, amantadine (40 mg/kg) or budipine (10 mg/kg) did not significantly alter extracellular DA. REB (10 mg/kg), PAROX (10 mg/kg) both increased cortical DA while CLOM (10 mg/kg) produced a decrease. When amantadine or budipine was administered 30 min before the antidepressants, DA increases were markedly greater than following the antidepressants alone. Chronically drug effects were studied at 4, 7, 14 and 21 days. Amantadine and budipine did not significantly alter extracellular DA at any time. The three antidepressants elicited a gradual increase in DA which became significant after 7 days and tended to plateau thereafter. When amantadine (20 mg/kg) or budipine (5 mg/kg) was co-administered with the three antidepressants, two differences were seen compared with the antidepressants alone. Firstly, the time required for significant increases in cortical DA was reduced with elevated levels now being observed by 4 days. Secondly, the increase in extracellular DA was greater in these rats throughout the experiment. If increased extracellular DA represents a step in the mechanism of action of antidepressants, these data suggest that combined treatment with clinically tolerated NMDA antagonists such as amantadine could reduce the delay in therapeutic onset of antidepressants and possibly enhance their efficacy.
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Type 1 diabetes is a rare but serious complication of interferon therapy. Repetitive treatment seems to facilitate this complication. Screening for islet antibodies before a second therapy could be useful.
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After a short summary of the leading symptoms, the neuropathological and the pathobiochemical findings in Parkinson's disease, the possibilities of pharmacological treatment are pointed out. The choice of the suitable medication depends on the stage and severity of the disorder and the leading symptoms. Medical side-effects and contraindications of the different antiparkinsonica must be considered. Problems of long-term medication especially of L-dopa are discussed. Examples of reasonable "combined therapies" are given allowing the attempt to reduce the L-dopa dose without losing treatment effectiveness. In addition to the pharmacological treatment and for special indications, surgical i.e. stereotactic manipulations, intensive physiosocial care, physiotherapy and logotherapy are very necessary.
Response to memantine therapy may include behavioral improvements allowing a dose-sparing effect of antipsychotic medication. Changes in psychoactive drug burden may be a valuable surrogate marker of memantine's effects on behavior.
After a patient is diagnosed with Parkinson disease (PD), there are many therapeutic options available. This article provides examples of prototypical patients encountered in clinical practice and illustrates the various pharmacologic and nonpharmacologic treatment options for the motor symptoms of PD.