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Pentacycloundecylamines (PCUs) and adamantane amines, such as NGP1-01 (1) and amantadine, have shown significant channel blocking activities. They are postulated to act as chemosensitizers and circumvent the resistance of the plasmodia parasite against chloroquine (CQ) by inhibiting the p-glycoprotein efflux pump and enabling the accumulation of CQ inside the parasite digestive vacuole. Twelve polycyclic amines containing either a PCU or adamantane amine moiety conjugated to different aromatic functionalities through various tethered linkers were selected based on their channel blocking abilities and evaluated as potential chemosensitizers. Compounds 2, 4, 5 and 10 showed significant voltage-gated calcium channel (VGCC) blocking ability (IC50=0.27-35 μM) and were able to alter the CQ IC50 in differing degrees (45-81%) in the multidrug resistant Plasmodium falciparum Dd2 isolate. Among them, the PCU-dansyl amine compound (4) displayed the best potential to act as a chemosensitizer against the Dd2 strain at a 1 μM concentration (RMI=0.19) while displaying moderate antiplasmodial activity (Dd2 IC50=6.25 μM) and low in vitro cytotoxicity against a mammalian cell line (CHO, IC50=119 μM). Compounds 2 and 10 also showed some promising chemosensitizing abilities (RMI=0.36 and 0.35 respectively). A direct correlation was found between the VGCC blocking ability of these polycyclic amines and their capacity to act as CQ resistance modulating agents.
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Physical methods were used to characterize sepia, synthetic, and bovine melanin. Their binding properties toward memantine were determined in deionized water and phosphate-buffered saline (PBS) at 37 degrees C. Melanin-memantine binding was measured indirectly by determining the unbound fraction of memantine. Curve fitting according to the Langmuir binding isotherm for one binding site was used for the determination of binding capacity (BLmax) and dissociation constant (KD).
Psychotic symptoms develop in 20-30% of patients with Parkinson's disease (PD) receiving chronic anti-PD medications, and visual hallucinations with or without delirium and paranoid delusions are the most frequent symptoms. Psychotic symptoms disturb ADL and QOL of PD patients and tax caregivers far more than the motor disabilities do, and good management of drug-induced psychotic symptoms is potentially important. Withdrawal of anti-PD drugs relieves the patients from psychotic side effects, but worsens the parkinsonian motor symptoms. The first step of treatment is to eliminate triggering factors other than anti-PD drugs, such as infections, metabolic disorders, subdural hematoma, and hallucinogenic drugs. The second step is to eliminate anti-PD drugs in the following order; first anticholinergics, amantadine and selegiline, second dopamine agonists, and finally levodopa/carbidopa. Anti-PD medications should be reduced to the point of improving psychotic side effects without drastically worsening parkinsonian motor symptoms. When the above adjustments fail to sufficiently alleviate psychotic side effects, the third step is consideration of antipsychotic drugs although they have potential capacity to antagonize dopamine D2 receptors and worsen parkinsonism. Atypical antipsychotics such as clozapine and olanzapine are recommended, though the former is not available in Japan.
The study group included 6 patients being treated for Parkinson disease who were referred for surgery at a tertiary medical center. After providing written informed consent, participants received intravenous amantadine sulfate 200 mg after induction of anesthesia and 24 hours later. The regular antiparkinsonian regimen was stopped immediately before surgery and restarted after surgery. Patients underwent a neurological evaluation with the Unified Parkinson Disease Rating Scale at 3 time points: preoperatively, 24 to 72 hours postoperatively, and 1 month postoperatively, and the scores were compared.
Washed microsomes from rabbit liver reduced 1-nitrosoadamantane to N-hydroxy-1-aminoadamantane in the presence of a cofactor solution under aerobic conditions; no further reduction of the hydroxylamino metabolite to 1-aminoadamantane (amantadine) occurred. Reduced pyridine nucleotide cofactors are needed for the metabolic reduction. The rate of formation of N-hydroxy-1-aminoadamantane depended upon the microsomal protein content, the time of incubation and the concentration of 1-nitrosoadamantane incubated. The metabolic reduction occurred in air as well as under nitrogen or carbon monoxide. Cupric chloride, mercuric chloride, cysteamine, FAD, and FMN decreased significantly the C-nitroso reductase. The properties of the C-nitroso reductase differed from those of other microsomal reductive pathways.
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Thirty-one common geriatric and AD symptoms from NH charts were scored based on their emergence or resolution (+1 or -1 points, respectively), worsening or improvement (+0.5 or -0.5 points, respectively), or absence of change (0 points), compared with the baseline period (the first 30 days analyzed in the charts, during which all residents received memantine treatment). Patients' weight change was also captured.
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Deficits in cholinergic and glutamatergic neurotransmission have been linked to the symptomatology of Alzheimer's disease, and current therapies for Alzheimer's, including cholinesterase inhibitors (ChEIs) and the N-methyl-d-aspartate receptor antagonist memantine, have been developed to compensate for these deficits. This article reviews the results of clinical trials involving agents approved by the United States Food and Drug Administration for use in the treatment of Alzheimer's disease (namely, ChEIs for mild to moderate Alzheimer's and memantine for moderate to severe Alzheimer's). In particular, the efficacy of current monotherapy strategies in the treatment of cognitive and functional symptoms of Alzheimer's disease will be addressed. In addition, data from a clinical trial examining the use of a ChEI in combination with memantine will also be discussed, as it has been hypothesized that ChEIs and memantine may offer synergistic benefits due to their distinct mechanisms of action.
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Data were extracted, pooled where possible, and weighted mean differences, standardized mean differences or odds ratios were estimated. Intention-to-treat (ITT) and observed cases (OC) analyses are reported, where data were available.
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The screening for antioxidative compounds for topical administration resulted in new, interesting findings. In the drug testings amantadine, bufexamac, tryptophan, melatonin, propranolol and hyaluronic acid were found to act antioxidatively whereas for ascorbic acid pro-oxidative effects were determined. Buckwheat extract significantly reduced the level of irradiation induced lipid peroxidation as well as the extracts of St. John's Wort, melissa and sage. The resistant starch novelose 330 and the samples of locust bean gum from a swing mill grinding series showed lipid protection after UV irradiation in the polysaccharide test rows.
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Currently, three predominant subtypes of influenza virus are prevalent in pig populations worldwide: H1N1, H3N2, and H1N2. European avian-like H1N1 viruses, which were initially detected in European pig populations in 1979, have been circulating in pigs in eastern China since 2007. In this study, six influenza A viruses were isolated from 60 swine lung samples collected from January to April 2011 in eastern China. Based on whole genome sequencing, molecular characteristics of two isolates were determined. Phylogenetic analysis showed the eight genes of the two isolates were closely related to those of the avian-like H1N1 viruses circulating in pig populations, especially similar to those found in China. Four potential glycosylation sites were observed at positions 13, 26, 198, 277 in the HA1 proteins of the two isolates. Due to the presence of a stop codon at codon 12, the isolates contained truncated PB1-F2 proteins. In this study, the isolates contained 591Q, 627E and 701N in the polymerase subunit PB2, which had been shown to be determinants of virulence and host adaptation. The isolates also had a D rather than E at position 92 of the NS1, a marker of mammalian adaptation. Both isolates contained the GPKV motif at the PDZ ligand domain of the 3' end of the NS1, a characteristic marker of the European avian-like swine viruses since about 1999, which is distinct from those of avian, human and classical swine viruses. The M2 proteins of the isolates have the mutation (S31N), a characteristic marker of the European avian-like swine viruses since about 1987, which may confer resistance to amantadine and rimantadine antivirals. Our findings further emphasize the importance of surveillance on the genetic diversity of influenza A viruses in pigs, and raise more concerns about the occurrence of cross-species transmission events.
This conference was organized according to the methodological rules published by the Agence Nationale d'Accréditation et d'Evaluation en Santé (ANAES). The conclusions and recommendations contained in this document were written, in full independence, by the jury of the conference. ANAES is in no way accountable for these views.
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Iminosugar derivatives are potential drugs for treatment of HCV infections.
Parkinson's disease is a movement disorder resulting from neurodegeneration of the basal ganglia. Parkinson's disease is usually diagnosed at approximately 55-60 years of age and affects approximately 1% of the population over 60 years. Dopaminergic cells located in the substantia nigra and whose terminals extend to the striatum degenerate slowly such that 60% of cells are already lost when clinical motor symptoms first become evident. In addition to the classic triad of Parkinson's disease symptoms, rest tremor, muscular rigidity and bradykinesia, abnormalities in postural reflexes, dementia and depression are important comorbid conditions. Current therapies are aimed primarily at replacing dopamine with the dopamine precursor L-dopa or by the use of direct acting dopamine receptor agonists. Adjunctive treatments with monoamine oxidase inhibitors, catechol-O-methyl transferase inhibitors and amantadine are also used. While providing very effective symptomatic therapy in early stages of the disease, these agents fail to halt disease progression. Thus, while these treatments generally provide excellent results for 2-5 years, quality of life for Parkinson's disease patients becomes increasingly poor 5-10 years after diagnosis. Symptoms that become increasingly problematic with disease progression include inconsistencies in motor control (response fluctuations), gait and balance abnormalities, cognitive loss, hypophonia and dysphagia. Therefore, in order to maintain an acceptable quality of life for patients with Parkinson's disease, therapies that provide not only symptomatic improvement, but also slow or stop disease progression are greatly needed. In this review, we will discuss possible mechanisms of cell death in Parkinson's disease and related potentially disease-modifying therapies. These therapies include dopaminergic cell tranplantation and the use of growth factors. Small molecules that may act as antioxidants, nicotinic receptor agonists, nitric oxide synthase inhibitors, immunophilins, excitatory amino acid-related (iGluR and mGluR agonists and antagonists) drugs and anti-inflammatory drugs will also be discussed.
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Drugs capable of inhibiting viruses in vitro were described in the 1950s, but real progress was not made until the 1970s, when agents capable of inhibiting virus-specific enzymes were first identified. The last decade has seen rapid progress in both our understanding of antiviral therapy and the number of antiviral agents on the market. Amantadine and ribavirin are available for treatment of viral respiratory infections. Vidarabine, acyclovir, ganciclovir, and foscarnet are used for systemic treatment of herpesvirus infections, while ophthalmic preparations of idoxuridine, trifluorothymidine, and vidarabine are available for herpes keratitis. For treatment of human immunodeficiency virus infections, zidovudine and didanosine are used. Immunomodulators, such as interferons and colony-stimulating factors, and immunoglobulins are being used increasingly for viral illnesses. While resistance to antiviral drugs has been seen, especially among AIDS patients, it has not become widespread and is being intensely studied. Increasingly, combinations of agents are being used: to achieve synergistic inhibition of viruses, to delay or prevent resistance, and to decrease dosages of toxic drugs. New approaches, such as liposomes carrying antiviral drugs and computer-aided drug design, are exciting and promising prospects for the future.
Despite subsidized access to CEDs in Australia, only a minority of people with AD was prescribed these drugs during the period of the study. It is likely that the combination of complex prescribing rules and negative perceptions about efficacy or cost-effectiveness might have contributed to these findings.
Sixty-one cocaine-dependent subjects participated in a double-blind, placebo-controlled trial of amantadine.
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Enhanced N-methyl-D-aspartate (NMDA) receptor function associated with a positive family history of alcoholism (FHP) has been hypothesized to contribute to the heritable risk for alcoholism. The objective of this study was to evaluate the relationship of alcoholism family history, NMDA receptor function, and cortical information processing by testing acute effects of the NMDA receptor antagonist memantine on event-related potential (ERP).
Motor fluctuations in Parkinson's disease (PD) typically develop after 4-6 years of therapy, and affect approximately half of all patients. The wearing-off effect is the most common type, and "delayed-on," "no-on," and "on-off" effects, as well as dyskinesias, may also develop as the disease progresses. Collectively, motor fluctuations represent a significant source of disability in advanced PD patients, and their mitigation is a major goal of patient management. Adjunctive medications, including dopamine agonists, amantadine, MAO-B inhibitors, and COMT inhibitors, each may reduce the frequency or duration of "off" periods, but none does so completely, and each contributes its own side effects which may limit optimal dosing. Surgery is another strategy to reduce "off" time, and both pallidotomy and deep brain stimulation of the globus pallidus or the subthalamic nucleus have been shown to be highly effective in this regard. However, surgery may be contraindicated in elderly advanced patients who could most benefit from its effect on "off" time. The unmet need for treatment of "off" episodes suggests the potential utility of an agent such as apomorphine injectable, which can reliably trigger an "on" response within 10-15 minutes of injection.
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Peroxyloxalate chemiluminescence is well established as a tool for improvement of selectivity and sensitivity for chemiluminophores and their derivations in HPLC eluates. Chemiluminescence in the far-red spectral region was investigated in this work to further enhance the sensitivity of chemiluminescence through more efficient singlet excitation energy transfer and to enhance the selectivity of the approach through a reduction in matrix and scatter interference. A number of fluorescent compounds that can be excited in the UV, visible and far red spectral regions were investigated for chemiluminescence yield using the bis(2,4,6-trichlorphenyl) oxylate reaction. It was found that a trend of increasing chemiluminescence with increasing excitation wavelength could be observed with cy5 providing the most efficient chemiluminescence. The succinate ester of cy5 was used to derivatize amantadine hydrochloride, an antiparkinsons drug, to form the derivative. The derivative was separated from reaction by products by C18 reversed phase HPLC and detected using a Soma S-3400 chemiluminescence detector. The detection limit for the diluted derivative was 200 femtomoles on column and sufficient for plasma analysis. Selectivity in plasma was demonstrated through derivatization of extracts of plasma that had been spiked with amantadine hydrochloride.
The review includes three trials, which were all at low risk of bias, involving 530 people with peripheral neuropathy. The effects of amantadine from one randomised, double-blind, placebo-controlled, cross-over trial comparing amantadine with placebo for the treatment of fatigue in 80 people with Guillain-Barré syndrome (GBS) were uncertain for the proportion of people achieving a favourable outcome six weeks post-intervention (odds ratio (OR) 0.56 (95% confidence interval (CI) 0.22 to 1.35, N = 74, P = 0.16). We assessed the quality of this evidence as low. Two parallel-group randomised double-blind, placebo-controlled trials comparing the effects of two doses of ascorbic acid with placebo for reducing fatigue in adults with Charcot-Marie-Tooth disease type 1A (CMT1A) showed that the effects of ascorbic acid at either dose are probably small (standardised mean difference (SMD) -0.12 (95% CI -0.32 to 0.08, n = 404, P = 0.25)) for change in fatigue after 12 to 24 months (moderate quality evidence). Neither ascorbic acid study measured fatigue at four to 12 weeks, which was our primary outcome measure. No serious adverse events were reported with amantadine. Serious adverse events were reported in the trials of ascorbic acid. However,risk of serious adverse events was similar with ascorbic acid and placebo.
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Impulse control disorders are a psychiatric condition characterized by the failure to resist an impulsive act or behavior that may be harmful to self or others. In movement disorders, impulse control disorders are associated with dopaminergic treatment, notably dopamine agonists (DAs). Impulse control disorders have been studied extensively in Parkinson's disease, but are also recognized in restless leg syndrome and atypical Parkinsonian syndromes. Epidemiological studies suggest younger age, male sex, greater novelty seeking, impulsivity, depression and premorbid impulse control disorders as the most consistent risk factors. Such patients may warrant special monitoring after starting treatment with a DA. Various individual screening tools are available for people without Parkinson's disease. The Questionnaire for Impulsive-Compulsive Disorders in Parkinson's Disease has been developed specifically for Parkinson's disease. The best treatment for impulse control disorders is prevention. However, after the development of impulse control disorders, the mainstay intervention is to reduce or discontinue the offending anti-Parkinsonian medication. In refractory cases, other pharmacological interventions are available, including neuroleptics, antiepileptics, amantadine, antiandrogens, lithium and opioid antagonists. Unfortunately, their use is only supported by case reports, small case series or open-label clinical studies. Prospective, controlled studies are warranted. Ongoing investigations include naltrexone and nicotine.
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Randomised controlled trials of participants with DS and AD in which treatment with memantine was administered compared with a placebo group.
Evidence of drug-related improvement of functions after stroke or TBI is still limited, either because of small and highly selected patient groups or due to conflicting results. Currently, most convincing evidence exists for piracetam for improvement of poststroke aphasia and amantadine for enhancing arousal and cognition after TBI. Some evidence can be found for improvement of stroke-related motor deficits by levodopa, enhanced speed of mental processing in TBI by methylphenidate and improvement of poststroke aphasia by dextroamphetamine. Large randomized controlled trials are needed to evaluate the effectiveness of serotonin reuptake inhibitors or noradrenaline reuptake inhibitors on motor functions.