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In this open-label study, participants receiving donepezil had better functional recovery than participants receiving galantamine or the historical comparators. This improvement may reflect efficacy at the starting dose for donepezil but not galantamine. A randomized trial is in progress.
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Among the 1,373 patients evaluated, 6% (N=81) were receiving ChEIs. They represented various stages of the disease, with cognitive and functional decline ranging from severe (18%) to very mild (10%). Among patients receiving ChEIs, 29% met neither the indication for which these drugs were approved, nor professional guidelines. Patient evaluation at entry was of high quality, with 90% of records including cognitive, functional and behavioural evaluation. Follow-up evaluations were weaker, with at least one assessment domain missing in 40% of the medical records. ChEIs treatment was maintained, although almost half of patients experienced a worsening of their clinical state.
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Alzheimer's disease (AD) is a chronic neurodegenerative disorder that leads to disturbances of cognitive functions. Although the primary cause of AD remains unclear, brain acetylcholine deficiency, oxidative stress and neuroinflammation may be considered the principal pathogenic factors. The present study was constructed to investigate the anti-amnestic effect of pyrrolidine dithiocarbamate (PDTC) on scopolamine-induced behavioral, neurochemical and biochemical changes in rats. PDTC (50 and 100mg/kg) and donepezil (2.5mg/kg) were orally administered for 14 successive days. Dementia was induced at the end of the treatment period by a single injection of scopolamine (20mg/kg; i.p.), and Y-maze test was conducted 30min thereafter. Rats were then sacrificed and homogenates of cortical and hippocampal tissues were used for the estimation of noradrenaline, dopamine, serotonin and heat shock protein 70 contents along with acetylcholinesterase activity. In addition, certain oxidative stress markers, pro-inflammatory and anti-inflammatory cytokines were assessed. Histological examination of cortical and hippocampal tissues was also performed. Scopolamine resulted in memory impairment that was coupled by alterations in the estimated neurotransmitters, heat shock protein 70, acetylcholinesterase activity, oxidative stress as well as inflammatory biomarkers. Histological analysis revealed serious damaging effects of scopolamine on the structure of cerebral cortex and hippocampus. Pretreatment of rats with PDTC in both doses mitigated scopolamine-induced behavioral, biochemical, neurochemical and histological changes in a manner comparable to donepezil. The observed anti-amnestic effect of PDTC makes it a promising candidate for clinical trials in patients with cognitive impairment.
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1) The administration of sildenafil (group II) and donepezil (group III) has favorable effects on reducing OS in experimentally induced CLLI. 2) Sildenafil and Donepezil administration stimulates extracellular AO defense on account of CP. 3) Sildenafil and Donepezil administration influences intracellular redox homeostasis on account of the GSH/GSSG couple, the major redox buffer in the body.
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The cholinergic hypothesis claims that a decrease of acetylcholine (ACh) in the brain of patients with Alzheimer's Disease (AD) plays an important role in the deterioration of cognitive functioning. This hypothesis has led to extensive research in possible therapeutic approaches towards improving cholinergic transmission in AD patients. The different approaches have focused on the following six strategies: ACh precursors, ACh release, M1, M3, or M4 receptor agonists, M2 receptor antagonists, nicotinic agonists, and acetylcholinesterase inhibitors (AChEI). The aim of this review is to assess the effectiveness of the cholinergic approach for the treatment of AD.
Cholinesterase inhibitors have similar cardiovascular risk profiles. Associations between memantine and fatal outcomes in Denmark may be related, in part, to selection of sicker individuals for memantine therapy.
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To determine whether donepezil hydrochloride can reduce the prevalence and severity of delirium in older adults undergoing hip fracture repair.
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After treatment, the scores for MMSE and ADL were improved in the combined acupuncture and medication group, the Chinese herb group and the western medicine group, which were better in the combined acupuncture and medication group (P < 0.05). The total effective rate of 85.7% in the combined acupuncture and medication group was better than 71.4% in the Chinese herb group and 67.9% in the western medicine group.
Nicotinic acetylcholine receptors and N-methyl-D-aspartate (NMDA) receptors are known to be down-regulated in the brain of patients with Alzheimer's disease. It was previously shown that the nootropic drugs nefiracetam and galantamine potentiate the activity of both nicotinic and NMDA receptors. We hypothesized that donepezil, a nootropic with a potent anticholinesterase activity, might also affect the NMDA system. NMDA-induced currents were recorded from rat cortical neurons in primary culture using the whole-cell patch-clamp technique at a holding potential of -70 mV in Mg2+-free solutions. In multipolar neurons, NMDA currents were decreased by bath and U-tube applications of 1 to 10 microM donepezil but were increased by 30 to 100 microM donepezil. Donepezil suppression occurred in a manner independent of NMDA concentrations ranging from 3 to 1000 microM. The donepezil suppression of NMDA currents was prevented by inhibition of protein kinase C (PKC) but unaffected by protein kinase A (PKA) and G proteins. In bipolar neurons, however, NMDA currents were potently augmented by bath and U-tube applications of 0.01 to 100 microM donepezil. Donepezil potentiation occurred at high NMDA concentrations that evoked the saturating responses and in a manner independent of NMDA concentrations ranging from 3 to 1000 microM. The potentiation of NMDA currents by donepezil was decreased by inhibition of PKC and abolished by modulation of G proteins but not by PKA inhibition. It was concluded that donepezil at low therapeutic concentrations (0.01-1 microM) potentiated the activity of the NMDA system and that this action together with cholinesterase inhibition would contribute to the improvement of learning, memory, and cognition in patients with Alzheimer's disease.
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We would suggest that more focused research into the effects of AChEI's on positive symptoms of schizophrenia, specifically visual hallucinations, is needed.
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Alzheimer's disease (AD) is the most common neurodegenerative disorder in the elderly, and studies have suggested that β-asarone has pharmacological effects on beta-amyloid (Aβ) injected in the rat hippocampus. However, the effect of β-asarone on autophagy in the APP/PS1 transgenic mouse is unreported. APP/PS1 transgenic mice were randomly divided into six groups (n=10/group): an untreated group, an Aricept-treated group, a 3-MA-treated group, a rapamycin-treated group, an LY294002-treated group, a β-asarone-treated group. The control group consisted of wild-type C57BL/6 mice. All treatments were administered to the mice for 30 days. Spatial learning and memory were assessed by water maze, passive avoidance, and step-down tests. AChE and Aβ42 levels in the hippocampus were determined by ELISA. p-Akt, p-mTOR, and LC3B expression were detected by flow cytometry. The expression of p-Akt, p-mTOR, Beclin-1, and p62 proteins was assessed by western blot. Changes in autophagy were viewed using a transmission electron microscope. APP and Beclin-1 mRNA levels were measured by Real-Time PCR. The learning and memory of APP/PS1 transgenic mice were improved significantly after β-asarone treatment compared with the untreated group. In addition, β-asarone treatment reduced AChE and Aβ42 levels, increased p-mTOR and p62 expression, decreased p-Akt, Beclin-1, and LC3B expression, decreased the number of autophagosomes and reduced APP mRNA and Beclin-1 mRNA levels compared with the untreated group. That is, β-asarone treatment can improve the learning and memory abilities of APP/PS1 transgenic mouse by inhibiting Beclin-1-dependent autophagy via the PI3K/Akt/mTOR pathway.
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Inhibition of acetylcholinesterase improves symptoms of dementia in patients with Parkinson's disease (PD). Dementia in PD has a cumulative incidence of up to 80% and is mainly caused by a distinct cholinergic deficit. Objectives of this investigator initiated multicenter open label trial were to confirm the efficacy of donepezil in the treatment of dementia in PD patients and to investigate the tolerability and safety of donepezil. The Mini Mental State Examination (MMSE)-score significantly increased in patients, who finished the trial. A detailed analysis of the various items of the MMSE revealed, that only task performance of orientation and recall significantly improved. Scores of the short syndrome test and the Clinical Global Impression Scale improved, motor impairment did not increase. Only 14 out of 24 PD patients finished the trial due to predominant onset of vomiting, nausea, dizziness and confusion. This may result from the titration regime of donepezil, that allows only 5 and 10 mg dosages. Participants with premature study termination had a significant longer duration of PD, less motivation and sleep disturbances at night. Treatment with donepezil was only effective in PD patients with dementia, who experience nearly no side effects from the drug.