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As part of the development of the Statistical Analysis Plan for the DOMINO trial, investigators met to consider expert opinion- and distribution-based values for the MCID and triangulated these to provide appropriate values for three outcome measures, the Standardised Mini-mental State Examination (sMMSE), Bristol Activities of Daily Living Scale (BADLS) and Neuropsychiatric Inventory (NPI). Only standard deviations (SD) were presented to investigators who remained blind to treatment allocation.
Two phase I, single-dose, randomized, open-label, crossover studies were conducted in 18- to 45-year-old healthy individuals. In MDX-PK-104 study, fasting participants (N = 38) received co-administered memantine ER and donepezil or the FDC. In MDX-PK-105 study, participants (N = 36) received three treatments: intact FDC taken while fasting or after a high-fat meal, or FDC contents sprinkled on applesauce while fasting. Standard pharmacokinetic parameters for memantine and donepezil were calculated from the plasma concentration time-curve using non-compartmental analyses. Linear mixed-effects models were used to compare: (a) FDC versus co-administered individual drugs; (b) FDC fasted versus with food; and (c) FDC sprinkled on applesauce versus FDC intact, both fasted. Safety parameters were also evaluated.
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Randomised and quasi-randomised studies comparing amantadine and/or rimantadine with placebo, control antivirals or no intervention, or comparing doses or schedules of amantadine and/or rimantadine in healthy adults.
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Age caused concurrent changes in the activation of the adenylate-cyclase activity by dopamine in the diencephalon and the stimulation of the basal level of cAMP by isoproterenol in the lymphocytes were demonstrated in the spontaneously tumor producing C3H mice. These changes may be related to the occurrence of tumors in these animals. The above-mentioned changes in the cAMP system were not found in AB mice. By treating the adult C3H mice with substances which increase the cAMP level, it was possible to achieve a renewed stimulation of the cAMP system as seen in young mice. With this treatment the spontaneous tumor-induction rate was also reduced. In the adenocarcinomas of the C3H mice a decrease in the level of prostaglandin E and an increase in the level of prostaglandin F2 alpha was observed.
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In the 2006-to-2007 influenza season, amantadine-sensitive strains were found among the N-lineage influenza A (H3N2) viruses, which were previously believed to be associated with amantadine resistance. Whole-genome sequencing results indicated that this was due to a further reassortment event.
Residents of two nursing homes with a total population of 301 individuals
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There have been numerous studies on the influence of ethanol on neurotransmitters, with conflicting results for the individual transmitters. It also refers to dopamine Hunt and Majchrowicz have found that dopamine circulation lowers after a prolonged administration of ethanol. The results of other experiments point out that such a long-lasting activity of ethanol has no influence on dopamine circulation. Tabakoff and Hoffman indicated that dopamine synthesis is lowered during the symptoms of ethanol abstinence. Griffiths et al. as well as Wajda et al. have proved that the level of dopamine in the striatum occurring at ethanol abstinence increases and comes back again to its initial value after 18 or 48 hrs. Fadda et al., while examining the prolonged influence of ethanol upon dopamine metabolism, has shown that after 24 hrs since the stop in ethanol administration, there has been an increase of dopamine level in the rat's frontal lobe of cortex cerebri. In other structures of the brain the dopamine level has not been changed. Darden and Hunt obtained the results showing a considerable decrease of dopamine liberation in the striatum during abstinence periods. In view of the biochemical research it is difficult to estimate explicitly the role of dopaminergic system in the appearance of dependence and symptoms of ethanol abstinence in the experimental animals. Some behavioral observations carried out on animals during the ethanol abstinence suggest that the prolonged administering of ethanol brings about hypofunction of central dopaminergic neurons.
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An FDC capsule containing 28 mg memantine ER and 10 mg donepezil is bioequivalent to commercially available memantine ER and donepezil, and bioavailability is not affected by food intake or sprinkling of capsule contents on applesauce.
Ts65Dn (TS) mice exhibit several phenotypic characteristics of human Down syndrome, including an increased brain expression of amyloid-beta protein precursor (AbetaPP) and cognitive disturbances. Aberrant N-methyl-D-aspartate (NMDA) receptor signaling has been suspected in TS mice, due to an impaired generation of hippocampal long-term potentiation (LTP). Memantine, an uncompetitive NMDA receptor antagonist approved for the treatment of moderate to severe Alzheimer's disease, is known to normalize LTP and improve cognition in transgenic mice with high brain levels of AbetaPP and amyloid-beta protein. It has recently been demonstrated that acute injections of memantine rescue performance deficits of TS mice on a fear conditioning test. Here we show that oral treatment of aged TS mice with a clinically relevant dose of memantine (30 mg/kg/day for 9 weeks) improved spatial learning in the water maze task and slightly reduced brain AbetaPP levels. We also found that TS mice exhibited a significantly reduced granule cell count and vesicular glutamate transporter-1 (VGLUT1) labeling compared to disomic control mice. After memantine treatment, the levels of hippocampal VGLUT1 were significantly increased, reaching the levels observed in vehicle treated-control animals. Memantine did not significantly affect granule cell density. These data indicate that memantine may normalize several phenotypic abnormalities in TS mice, many of which--such as impaired cognition--are also associated with Down syndrome and Alzheimer's disease.
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These findings suggest that the NMDA receptor may play a key role in the earliest stages of opiate dependence and provide further evidence that memantine may be useful for the treatment of opiate withdrawal.
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Dementia with Lewy-bodies (DLB) and Parkinson's disease dementia (PDD) are no rare causes of dementia. Both have neuropathologically, clinically, and neurochemically much in common. In the course of both conditions frequently psychotic symptoms occur, often induced by antiparkinsonian medication. Treatment of psychotic features with conventional antipsychotics is not tolerated in many cases. Therefore low-dose clozapine treatment is acknowledged usual practise for psychosis in Parkinson's disease and a case report indicates efficacy for psychosis in DLB, too. All other atypical antipsychotics except risperidone are not licensed for dementia in Germany, but risperidone is contraindicated in DLB due to manufacturer's notice and usually not well tolerated in DLB and Parkinson's disease. Open trials indicate safety for treatment of psychosis in DLB and PDD with quetiapine. Randomized controlled trials indicate, that quetiapine is less effective than clozapine against psychotic symptoms in both conditions, although comparatively safe. Cholinesterase inhibitors, especially rivastigmine, are a therapeutic alternative for treating both psychotic and cognitive symptoms in both conditions. Parkinsonism in DLB-patients responds worse to levodopa compared to patient with Parkinson's disease. Anticholinergic drugs often induce delirium in demented patients and therefore should be avoided. The same problem is associated with dopamine agonists in PDD and DLB. Amantadine, a NMDA-receptor antagonist like memantine, potentially bears the same risk of worsening psychotic symptoms. The following preliminary recommendation for drug treatment of PDD and DLB can be given: Stop all anticholinergic medication and reduce levodopa and other antiparkinsonian medication to the tolerated minimum. Levodopa alone is preferred. Treat with cholinesterase inhibitors to the maximum tolerated dose. If there is no adequate response regarding psychotic symptoms, add quetiapine. If this approach fails, replace quetiapine by low-dose clozapine. If behavioural disturbances are due to depression, anxiety, or irritability, treatment with an antidepressant, preferably citalopram, is an option.
1. By the use of the everted jejunal sac it was shown that chronic oral treatment of rats with various drugs can either increase or decrease the mucosal transport of (14)C-L-DOPA or alter its serosal/tissue ratio.2. (14)C-L-DOPA transport was significantly increased in rats that were chronically treated with L-DOPA and diminished in those that were treated with chlorpromazine and phenobarbitone.3. Chronic treatment with amantadine and neomycin did not affect (14)C-L-DOPA intestinal transport, although direct addition of amantadine to the medium, significantly increased (14)C-L-DOPA transport in everted sacs of nontreated rats. Addition of neomycin directly to the medium did not affect (14)C-L-DOPA transport.4. The possible mechanisms of these findings and their clinical significance are discussed.
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Adult male Wistar rats were trained to discriminate 0.6 mg/kg nicotine from saline under a two-lever, fixed-ratio 10 schedule of food reinforcement. During test sessions, injections of (+)MK-801 (0.03--0.3 mg/kg, i.p.), dextromethorphan (30 mg/kg, s.c.), or memantine (1--10 mg/kg, i.p.) were co-administered with s.c. nicotine (0.075--0.6 mg/kg; interaction tests) or saline (generalization tests). Additional interaction and generalization tests were conducted with the selective nicotinic receptor antagonists mecamylamine (0.1--3 mg/kg, s.c.) and MRZ 2/621 (0.3--10 mg/kg, i.p.), and the mGlu5 receptor antagonist MPEP (3--10 mg/kg, i.p.).
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To conduct a cost-effectiveness analysis comparing the addition of memantine to standard care (that is, without acetylcholinesterase inhibitors) with standard care alone in moderate-to-severe Alzheimer disease (AD) in Canada.
Thirty New Zealand White rabbits were divided into 5 different groups of 6 rabbits. Groups 60-7 and 60-5 received oral memantine 60 mg once a day for 7 and 5 days, respectively, and groups 30-5 and 30-3 received oral memantine 30 mg once a day for 5 and 3 days, respectively, all before surgery. Group C (control) received normal feeds without memantine. A paraplegic model was created by clamping both the aorta and the inferior vena cava infrarenally and just proximal to their bifurcations for 45 minutes. The modified Tarlov score, motor evoked potential (MEP), serum memantine concentration, and histopathology of the spinal cord were evaluated.
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Influenza surveillance comprises four components, three of which provide weekly data from October through May: a) state and territorial epidemiologists provide estimates of local influenza activity; b) approximately 140 sentinel physicians report their total number of patient visits and the number of cases of influenza-like illness; and c) approximately 70 collaborating laboratories of the World Health Organization (WHO) report weekly influenza virus isolations and submit selected influenza isolates to CDC for antigenic analysis. Throughout the year, vital statistics offices of 121 cities report deaths related to pneumonia and influenza (P&I), providing an index of the impact of influenza on mortality.
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These results provide empirical support for conducting a further study on comparing different add-on strategies for treating drug-induced SD.
The European Association for the Study of the Liver (EASL) International Consensus on Hepatitis C made by 72 experts in hepatology, epidemiology and virology at the EASL Consensus Conference, Paris, February, 1999 and confirmed by the 34th EASL Annual Meeting, Naples, 8-12 april 1999, is widely reviewed. Some newest and more effective strategies for treatment of the chronic viral hepatitis C were discussed during the Naples EASL meeting. Higher doses interferons (interferon-alpha or consensus interferon) plus ribavirin (or combination ribavirin and amantadine) for a longer period--12 months, improved efficacy of the treatment of chronic hepatitis C. An ultrarapid HCV clearance by daily hgh-dose interferon-alpha induction therapy in the start of the management plus ribavirin was achieved and discussed in naive patients and in nonresponders to standard therapy. A gene therapy by an effective genetic vaccine against HCV infection was widely discussed, too. Hepatitis C is an enormous present and future health burden to the world. Not until 2010, the most of therapeutic problems in patients with chronic persisted HCV infection would be resolved.
The inclusion criteria for all randomised controlled trials were that they should focus on the use of dopamine agonists on the treatment of cocaine dependence. Trials including patients with additional diagnosis such as opiate dependence were also eligible.
There were no significant differences between the two groups with respect to age, gender, nausea and vomiting, sleep quality, blood pressure, and heart rate. No significant differences were observed between the two groups in pain scores (P = 0.39) and analgesic consumption (P = 0.78).
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OH was significantly related to older age, polypharmacy and amantadine or diuretics intake, while entacapone exposure appeared to reduce the risk of OH. Low concordance between OH and orthostatic symptoms was observed.
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The late 1990s were a period of unprecedented activity in the development of new and much superior antivirals for the treatment of influenza infections. However, during the past 2 to 3 years and largely for commercial reasons, there has been a decline in interest in their further development by major drug companies. This situation may soon change with the possible advent of new pandemic viruses, and moves are afoot in several countries to consider the stockpiling of antivirals. The neuraminidase inhibitors zanamivir and oseltamivir, and the M2 inhibitors amantadine and rimantadine, remain the only options for controlling respiratory disease caused by influenza viruses, although the latter two could not be used against very recent H5N1 strains. There are several other neuraminidase inhibitors in development. Compounds with activity against other respiratory viruses, notably rhinoviruses, are also in development, many based on a newer knowledge of viral protein structure and function (rational drug design).
Cognitive dysfunction is very common in multiple sclerosis (MS) and it severely impairs patients' quality of life. Thus, we explored whether memantine might improve cognitive performance in patients with MS.
Parkinson's disease (PD), a common neurodegenerative disorder caused by the loss of the dopaminergic input to the basal ganglia, is commonly treated with l-DOPA. Use of this drug, however, is severely limited by the development of dystonic and choreic motor complications, or dyskinesia. This chapter describes the molecular mechanisms implicated in the emergence and manifestation of l-DOPA-induced dyskinesia (LID). Particular emphasis is given to the role played in this condition by abnormalities in signal transduction at the level of the medium spiny neurons (MSNs) of the striatum, which are the principal target of l-DOPA. Recent evidence pointing to pre-synaptic dysregulation is also discussed.
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Because of the described immunosuppressive potency of 1-aminoadamantan, the authors prepared conjugates of N-substituted 1-aminoadamantan derivatives with human serum albumin (HSA) and bovine gamma globulin (BGG). To achieve covalent binding of 1-aminoadamantan (1) to HSA and BGG (following the isothiocyanate procedure), 1 was converted to the N-(p-isothiocyanatobenzoyl) derivative of 1-aminoadamantan (4) via the nitro compound (2) and the amino compound (3). The reaction of 4 with HSA and BGG yielded conjugates with thiourea structure. The imidic acid ester hydrochloride (7) and the thioimidic acid ester hydrochloride (11) were prepared from the N-(p-cyanobenzoyl) derivative of 1-aminoadamantan (6) and reacted with HSA and BGG to give conjugates with amidine structure.