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The study involved 1516 patients (1386 of whom were evaluable) who had been diagnosed with Alzheimer-type dementia (ATD) according to the criteria in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV); these patients, who were selected by 157 participating physicians (neurologists, psychiatrists and geriatricians), gave their informed written consent and had been receiving treatment with rivastigmine solution over the past six months. The main variable was the rivastigmine solution treatment regimen and the secondary variables included socio-demographic data, health care data and the researcher's overall clinical impression from the time treatment was begun, among others.
BCHE-K carriers showed a lower responder rate on the ADAS-cog than non-carriers (38.2 vs. 61.7%, p = 0.02), and this trend was evident in AD patients with apolipoprotein E ε 4 (35 vs. 60.7%, p = 0.001). The presence of the BCHE-K allele predicted a worse response on the ADAS-cog (odds ratio 0.35, 95% confidence interval 0.14-0.87), after adjusting for demographic and baseline cognitive and functional variables.
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Alzheimer disease(AD) is characterized as neurodegenerative disease showing impairment of cognitive function, death of neuronal cells, numerous numbers of senile plaques and tangle of neurofilaments. There are two different hypotheses that neurotoxicity of aggregated amyloid beta protein(A beta) and hyperphosphorylation of tau protein are the causes of AD. The dysfunction of cholinergic neuronal system is observed in the early stage of AD. Therefore, the strategy to increase of acetylcholine (ACh) level in brain by using ACh esterase inhibitor is mainstream in the present. We have tacrine, donepezil, rivastigmine and galantamine. Tacrine, the first drug for AD, is replaced by other drugs, because of its hepatic toxicity. Galantamine binds allosteric sites of nicotine receptor and stimulates it in addition to its inhibitory effect on ACh esterase. Metamantine was approved in EU in 2002. It is non-competitive inhibitor of NMDA receptors, and dopamine releaser, which has neuroprotective effect. All of the above drugs improve cognitive function of patients, and they could delay hospitalization for 7 months or more. In the present anti-inflammatory drugs, anti-oxidative drugs and estrogen are under investigation. As anti-A beta therapy, inhibitors of beta -and gamma-secretase, A beta aggregation inhibitors, A beta degradation stimulators and A beta vaccination are possible strategies. The inhibitors of tau protein phosphorylation and activators of phosphates could be that of anti-tau protein phosphorylation. Additionally, it is expected to have the strategies such as neuroregeneration by neurotorophic factors and immunopyline ligands, and supply of neuronal cells by gene therapy and human ES cells.
To estimate the cost effectiveness (from the UK NHS and personal social services perspective) of the cholinesterase inhibitors donepezil, rivastigmine and galantamine compared with usual care in the treatment of mild to moderately severe Alzheimer's disease. Patients had a mean age of 74 years, a mean disease duration of 1 year and a mean Alzheimer's disease assessment scale-cognitive subscale score of 24.
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Drugs with potential cardiac adverse effects are commonly prescribed in Parkinson's disease (PD). To describe demographic and clinical characteristics in a group of PD patients with cardiac events and to evaluate risk factors.
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Trials selected were randomized, double-blind, parallel-group, and unconfounded comparisons of galantamine with placebo for a treatment duration of greater than 4 weeks in subjects with AD.
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There is ample evidence that the poststroke confusion syndrome or delirium is a manifestation of cholinergic deficit. Given this conception, we conducted a controlled study of efficacy and safety of acetylcholinesterase inhibitor rivastigmine in patients developed a delirium in the acute phase of ischemic stroke. The study included 224 consecutive stroke patients: 68 patients developed a delirium in the acute phase of disease. Severity of delirium was scored with the Delirium Rating Scale (DRS). A main group included 21 patients with delirium treated with rivastigmine in individually tailored doses. A control group included 47 patients with delirium who received only vascular and anticoagulant treatment, i.e. haloperidol. Cognitive functions were tested 3 and 6 months after stroke with the MMSE, the FAB, the Luria 10 point verbal test. The Zarit Burden Interview (ZBI) was used after 3 and 6 months to measure caregiver burden. In patients treated with rivastigmine, the delirium phase was significantly shorter (p<0,001) compared to the control group. In patients without delirium in the acute phase of stroke, the results of neuropsychological study were better (p<0,001) than in patients with delirium. Total ZBI scores were more favorable in the rivastigmine group than in the control one (p<0,05). To the end of the study, 5 patients died in the rivastigmine group, 17 patients in the control group and 3 patients in the group without delirium. Rivastigmine was safe in the acute phase of stroke patients even after the rapid titration.
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Alzheimer's disease is associated with a substantial economic impact on patients, their caregivers and society. Due to the current rise in the aging population, the prevalence and impact of Alzheimer's disease are expected to increase greatly. The cost of caring for someone with Alzheimer's disease is magnified in the more severe stages of the disease. There are four cognitive enhancers commonly used for the treatment of Alzheimer's disease: three cholinesterase inhibitors (donepezil, rivastigmine and galantamine) and one NMDA receptor antagonist (memantine). Of these, donepezil and memantine have been approved in many countries as pharmacological treatments for moderate to severe Alzheimer's disease, while donepezil, rivastigmine and galantamine are approved treatments for mild to moderate Alzheimer's disease. While cost effectiveness has been well studied in mild to moderate Alzheimer's disease, the cost-benefit information for drug therapy in moderate to severe Alzheimer's disease is less clear. This article reviews the pharmacoeconomic data available on these four drugs, with a specific focus on moderate to severe Alzheimer's disease, including economic burden, cost drivers, clinical outcomes and pharmacoeconomic studies. A key driver of the cost of Alzheimer's disease is the severity of the disease, indicating that the ability to stabilize the disease state is a potential source of cost savings. Drug therapies that can limit increases in behavioural problems and cognitive and functional impairment, and postpone institutionalization without an increase in longevity may serve to reduce the economic burden on Alzheimer's disease patients. The data suggest that, while the available, approved agents offer only modest improvements in clinical outcomes, they could be cost-effective treatments for moderate to severe Alzheimer's disease when viewed from the societal perspective. For memantine and donepezil, data are available that suggest that the cost of these drugs is offset by the clinical and societal benefits provided by slowing the progression of Alzheimer's disease. While there are few head-to-head comparison trials, the similarity in costs of the treatments and efficacy against placebo suggest that cost effectiveness will not be substantially different among treatments. More studies that examine longitudinal resource utilization and its relationship to drug treatment in the moderate to severe stages are needed to clarify cost benefit in this population and possibly differentiate between individual medications.
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Low education has been shown to be a risk factor for dementia. However, little is known about the association between educational level and dementia drugs.
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Many factors could be responsible for the different response to treatment with the cholinesterase inhibitors (ChEIs) donepezil and rivastigmine in Alzheimer's disease (AD) patients. Sex and the variants of the estrogen receptor α (ESR1) gene are reported to modulate AD susceptibility or the course of the disease. The aim of the present study was to verify whether patient's sex and ESR1 genotype could influence the response to ChEI treatment, as there is evidence that estrogens affect cholinergic system functioning.
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AN680 is very effective in preventing DSS-induced UC in mice and may therefore have potential therapeutic application in humans. Addition of ChE inhibition and indirect activation of α7nAChR lessens the efficacy of AN917 in this model.
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DL0410 ameliorates cognitive deficit and exerts neuronal protection in AD models, implicating this compound as a candidate drug for the prevention and therapy of AD.