Cognitive Benefits In Patients Research Articles

The Sound of Memory: Investigating Music Therapy's Cognitive Benefits in Patients with Dementia-A Network Meta-Analysis of Randomized Controlled Trials.

Numerous previous studies have shown the effectiveness of music therapy in enhancing cognitive functions in patients with dementia. Despite this, robust evidence in this field, especially concerning the comparison of different music therapy types, is lacking. Therefore, randomized controlled trials (RCTs) focusing on music therapy and cognitive functions in dementia patients, termed by "music" AND "dementia" OR "Alzheimer's disease" AND "cognitive", were identified from primary electronic databases to conduct this network meta-analysis (NMA). The primary outcome focused on the impact on cognitive functions, and the secondary outcome was the comparison of dropout rates between the intervention groups and the usual care control groups. Standardized mean difference (SMD) values and the corresponding 95% confidence intervals (CIs) were computed for effect evaluation. This study protocol has been registered in IPLASY (INPLASY202430082). A total of 14 RCTs with 1056 participants were enrolled, examining interventions including Active Music Therapy (AMT), Active Music Therapy with Singing (AMT + Sing), Rhythmic Music Therapy (RMT), Listening to Music (LtM), and Singing (Sing). The results indicated that RMT, AMT + Sing, and AMT all significantly improve cognitive functions in dementia patients, of which the SMD were 0.76 (95% CI = 0.32-1.21), 0.79 (95% CI = 0.03-1.49), and 0.57 (0.18-0.96), respectively. Compared with the control group (usual care), no music therapy type was associated with an increased dropout risk. In conclusion, music therapy can improve cognitive functions in patients with dementia without increasing the risk of dropout, particularly RMT, AMT + Sing, and AMT.

Exploring the Influence of Gut-Brain Axis Modulation on Cognitive Health: A Comprehensive Review of Prebiotics, Probiotics, and Symbiotics.

Recent research exploring the relationship between the gut and the brain suggests that the condition of the gut microbiota can influence cognitive health. A well-balanced gut microbiota may help reduce inflammation, which is linked to neurodegenerative conditions. Prebiotics, probiotics, and symbiotics are nutritional supplements and functional food components associated with gastrointestinal well-being. The bidirectional communication of the gut-brain axis is essential for maintaining homeostasis, with pre-, pro-, and symbiotics potentially affecting various cognitive functions such as attention, perception, and memory. Numerous studies have consistently shown that incorporating pre-, pro-, and symbiotics into a healthy diet can lead to improvements in cognitive functions and mood. Maintaining a healthy gut microbiota can support optimal cognitive function, which is crucial for disease prevention in our fast-paced, Westernized society. Our results indicate cognitive benefits in healthy older individuals with probiotic supplementation but not in healthy older individuals who have good and adequate levels of physical activity. Additionally, it appears that there are cognitive benefits in patients with mild cognitive impairment and Alzheimer's disease, while mixed results seem to arise in younger and healthier individuals. However, it is important to acknowledge that individual responses may vary, and the use of these dietary supplements should be tailored to each individual's unique health circumstances and needs.

A multimeal paradigm producing a low glycemic response is associated with modest cognitive benefits relative to a high glycemic response: a randomized, crossover trial in patients with type 2 diabetes

BackgroundType 2 diabetes (T2DM) and poor glucose regulation in the immediate postprandial period are both associated with impairments in cognitive function. There is evidence that foods that generate a better postprandial glycemic response, such as low GI foods (which produce a lower glycemic peak, less variability, and a more sustained decline), are associated with cognitive benefits over the morning. However, the potential impact of consuming multiple meals of this nature over the course of a day on cognition in T2DM has not been explored. ObjectivesThe primary aim of this research was to investigate whether a multimeal paradigm producing a low glycemic response was associated with cognitive benefits in patients with noninsulin-dependent T2DM relative to a multimeal paradigm producing a high glycemic response. MethodsTwenty-five adults with noninsulin-dependent T2DM (mean age: 57 y) consumed 2 multimeal profiles consisting of a breakfast, lunch, and afternoon snack on 2 separate test days following a randomized, counterbalanced, crossover design. The 2 conditions were a low GI profile (LGIP) and a high GI profile (HGIP). ResultsCognitive function, glycemic response, mood, and satiety were assessed over the day from 8:30 to 17:00. Overall, there were limited cognitive effects. However, there was evidence for cognitive benefits in the period before lunch, as demonstrated by better global cognitive and executive functions for the LGIP relative to the HGIP. No clear effects were observed for mood. ConclusionsThis study shows that a multimeal paradigm producing a low glycemic response was associated with some benefits for cognitive function in patients with T2DM. Clinical Trail Registry referenceNCT03360604 (clinical trial.gov).

Nutritional treatments for Alzheimer’s disease: A narrative review

AbstractBackgroundKnowledge is limited about ways to treat, manage and slow the progression of Alzheimer’s Disease (AD). It is suspected that there are potential nutrition‐related components that may contribute to the pathology of AD. This includes nutrient deficiencies and/or dietary factors that may lead to comorbidities, increasing the risk for development. Thus, many nutrient‐specific, dietary and medical food treatments are continually being researched. Some studies even combine both nutrient and dietary interventions to treat AD. The purpose of this review is to explore and discuss the efficacy of several macro‐ and micronutrients, antioxidants, dietary therapies and combined components to treat or slow the progression of AD while providing valuable insight into the role that nutrition may play in the treatment of this disease.MethodsUsing PubMed, Google Scholar, EBSCOhost and Science Direct, databases were searched using pertinent keywords. A total of 33 research articles were included, primarily consisting randomized, double‐blind, placebo‐controlled clinical human research trials with the addition of few animal studies. Full‐text studies in detail were obtained, assessed with data extracted and summarized.ResultsOverall, it was determined that folate in conjunction with Donepezil, may improve cognitive function and inflammatory markers. Omega‐3 fatty acids (FA) with ɑ‐lipoic acid may reduce cognitive and functional decline rates. Adequate B‐vitamin status is needed to obtain the benefits of omega‐3 FAs. Vitamin D supplementation and medical food Souvenaid may be considered for cognitive benefits in patients with AD. Medium‐chain triglyceride (MCT) supplementation is not yet supported. Antioxidant treatment is not recommended as it may accelerate cognitive decline. DASH, Mediterranean Diet, MIND and ketogenic diet therapy may be considered as dietary treatments in AD patients. Nutrient supplementation requires more research to determine appropriate dosages.ConclusionAlzheimer’s disease remains a major health concern to the aging public. The anti‐inflammatory properties, antioxidative and neuroprotective effects of several nutrition‐related treatments have been shown to be beneficial in combating the progression of this disease. Patient individualization must be considered prior to treating. It is recommended that future studies determine appropriate dosage amounts to minimize adverse effects.

Cognitive Enhancement of Repetitive Transcranial Magnetic Stimulation in Patients With Mild Cognitive Impairment and Early Alzheimer's Disease: A Systematic Review and Meta-Analysis.

Repetitive transcranial magnetic stimulation (rTMS), a non-invasive brain stimulation technique, has been considered as a potentially effective treatment for the cognitive impairment in patients with mild cognitive impairment (MCI) and Alzheimer’s Disease (AD). However, the effectiveness of this therapy is still under debate due to the variety of rTMS parameters and individual differences including distinctive stages of AD in the previous studies. The current meta-analysis is aiming to assess the cognitive enhancement of rTMS treatment on patients of MCI and early AD. Three datasets (PubMed, Web of Science and CKNI) were searched with relative terms and finally twelve studies with 438 participants (231 in the rTMS group and 207 in the control group) in thirteen randomized, double-blind and controlled trials were included. Random effects analysis revealed that rTMS stimulation significantly introduced cognitive benefits in patients of MCI and early AD compared with the control group (mean effect size, 1.17; 95% CI, 0.76 - 1.57). Most settings of rTMS parameters (frequency, session number, stimulation site number) significantly enhanced global cognitive function, and the results revealed that protocols with 10 Hz repetition frequency and DLPFC as the stimulation site for 20 sessions can already be able to produce cognitive improvement. The cognitive enhancement of rTMS could last for one month after the end of treatment and patients with MCI were likely to benefit more from the rTMS stimulation. Our meta-analysis added important evidence to the cognitive enhancement of rTMS in patients with MCI and early AD and discussed potential underlying mechanisms about the effect induced by rTMS.

Effects of Ketone Bodies on Brain Metabolism and Function in Neurodegenerative Diseases.

Under normal physiological conditions the brain primarily utilizes glucose for ATP generation. However, in situations where glucose is sparse, e.g., during prolonged fasting, ketone bodies become an important energy source for the brain. The brain’s utilization of ketones seems to depend mainly on the concentration in the blood, thus many dietary approaches such as ketogenic diets, ingestion of ketogenic medium-chain fatty acids or exogenous ketones, facilitate significant changes in the brain’s metabolism. Therefore, these approaches may ameliorate the energy crisis in neurodegenerative diseases, which are characterized by a deterioration of the brain’s glucose metabolism, providing a therapeutic advantage in these diseases. Most clinical studies examining the neuroprotective role of ketone bodies have been conducted in patients with Alzheimer’s disease, where brain imaging studies support the notion of enhancing brain energy metabolism with ketones. Likewise, a few studies show modest functional improvements in patients with Parkinson’s disease and cognitive benefits in patients with—or at risk of—Alzheimer’s disease after ketogenic interventions. Here, we summarize current knowledge on how ketogenic interventions support brain metabolism and discuss the therapeutic role of ketones in neurodegenerative disease, emphasizing clinical data.

Medications Used for Cognitive Enhancement in Patients With Schizophrenia, Bipolar Disorder, Alzheimer's Disease, and Parkinson's Disease.

Cognitive impairment, which frequently occurs in patients with schizophrenia, bipolar disorder, Alzheimer's disease, and Parkinson's disease, has a significant impact on the daily lives of both patients and their family. Furthermore, since the medications used for cognitive enhancement have limited efficacy, the issue of cognitive enhancement still remains a clinically unsolved challenge. We reviewed the clinical studies (published between 2007 and 2017) that focused on the efficacy of medications used for enhancing cognition in patients with schizophrenia, bipolar disorder, Alzheimer's disease, and Parkinson's disease. Acetylcholinesterase inhibitors and memantine are the standard treatments for Alzheimer's disease and Parkinson's disease. Some studies have reported selective cognitive improvement in patients with schizophrenia following galantamine treatment. Newer antipsychotics, including paliperidone, lurasidone, aripiprazole, ziprasidone, and BL-1020, have also been reported to exert cognitive benefits in patients with schizophrenia. Dopaminergic medications were found to improve language function in patients with Parkinson's disease. However, no beneficial effects on cognitive function were observed with dopamine agonists in patients with schizophrenia. The efficacies of nicotine and its receptor modulators in cognitive improvement remain controversial, with the majority of studies showing that varenicline significantly improved the cognitive function in schizophrenic patients. Several studies have reported that N-methyl-d-aspartate glutamate receptor (NMDAR) enhancers improved the cognitive function in patients with chronic schizophrenia. NMDAR enhancers might also have cognitive benefits in patients with Alzheimer's disease or Parkinson's disease. Raloxifene, a selective estrogen receptor modulator, has also been demonstrated to have beneficial effects on attention, processing speed, and memory in female patients with schizophrenia. Clinical trials with larger sample sizes evaluating comprehensive cognitive domains are warranted to examine the efficacy of medications in cognitive enhancement in patients with schizophrenia, bipolar disorder, Alzheimer's disease, and Parkinson's disease.

Pharmacotherapy for Vascular Cognitive Impairment.

Vascular cognitive impairment (VCI) is the second most common type of dementia after Alzheimer's disease (AD). Stroke and cardiovascular risk factors have been linked to both AD and VCI and potentially can affect cognitive function in mid and later life. Various pharmacological agents, including donepezil, galantamine, and memantine, approved for the treatment of AD have shown modest cognitive benefits in patients with vascular dementia (VaD). However, their functional and global benefits have been inconsistent. Donepezil has shown some cognitive benefit in patients with VaD only, and galantamine has shown some benefit in mixed dementia (AD/VaD). The benefits of other drugs such as rivastigmine, memantine, nimodipine, and piracetam are not clear. Some other supplements and herbal therapies, such as citicoline, actovegin, huperzine A, and vinpocetine, have also been studied in patients with VaD, but their beneficial effects are not well established. Non-drug therapies and lifestyle modifications such as diet, exercise, and vascular risk factor control are important in the management of VCI and should not be ignored. However, there is a need for more robust clinical trials focusing on executive function and other cognitive measures and incorporation of newer imaging modalities to provide additional evidence about the utility of these strategies in patients with VCI.

TREATMENT OF COGNITION

Treatment with cholinesterase inhibitors modestly improves cognition, activities of daily living and global clinician rating of patients with mild, moderate and severe Alzheimer's disease (AD). Improvements are close to minimal clinically important values such that clinicians should not expect to be able to make decisions about response in an individual treated patient. Treatment decisions will often be influenced by experience of side-effects, in particular nausea, vomiting, diarrhoea, vivid dreams and cramps. These drugs do not improve non-cognitive AD symptoms and there is no convincing evidence for additional cognitive or functional benefit with higher than standard (>10mg donepezil) dosing. Although most trials have been of short duration, treatment benefits appear to be sustained, even in severely affected individuals, and this should be considered in discontinuation decisions. Meta-analyses report cognitive benefits in patients with dementia with Lewy bodies and Parkinson's disease dementia. Although not recommended for patients with frontotemporal or vascular dementia, patients with mixed vascular and AD pathology may benefit from treatment. Memantine improves cognition, activities of daily living and global rating, but benefits are smaller than those seen with cholinesterase inhibitors, often not reaching clinically important levels and is often used for patients who cannot tolerate a cholinesterase inhibitor. Combination treatment with a cholinesterase inhibitor is associated with very small additional benefit compared to cholinesterase inhibitor alone. Cognitive stimulation therapy has better evidence to support claims for improving cognition in AD than cognitive training and cognitive rehabilitation. It is important to bear in mind that most cognitive intervention studies have not included active control interventions or strategies to blind outcome assessors that would allow meaningful comparison with the results of pharmaceutical trials. Finally, physical exercise may improve activities of daily living in AD, but reported effects on cognition have not been consistent. Together with the difficulties in interpretation of efficacy associated again with failure to include adequate control interventions or to blind outcome assessors, it is still unclear whether the intensity of prescribed exercise needs to exceed a threshold above which cognitive benefits can be demonstrated.

Cardiac rehabilitation is associated with lasting improvements in cognitive function in older adults with heart failure.

Heart failure (HF) is a known risk factor for cognitive impairment. Cardiac rehabilitation (CR) may attenuate poor neurocognitive outcomes in HF via improved physical fitness--a significant promoter of cognitive function. However, no study has examined the possible acute and lasting benefits of CR on cognitive function in persons with HF. Fifty-two patients with HF completed a 12-week Phase II CR program. All participants were administered neuropsychological testing and completed a brief physical fitness assessment at baseline, completion of CR (i.e. 12 weeks), and 12-month follow-up. Repeated measures analyses showed a significant time effect for both attention/executive function and memory (P < 0.05). Attention/executive function performance increased from baseline to 12 weeks and these gains remained up to 12 months; memory was unchanged from baseline to 12 weeks, but then improved between the 12-week and 12-month time points. Physical fitness improved from baseline to 12 weeks and these benefits were maintained 12 months later. Changes in physical fitness and cognitive function over time did not reach a statistically significant association, though poorer physical fitness was associated with decreased cognitive performance at the baseline and 12-month time points. CR is associated with both acute and lasting cognitive benefits in patients with HF. Prospective studies with extended follow-ups are needed to clarify the mechanisms that underpin cognitive improvements following CR (e.g., improved cerebral perfusion) and whether CR can ultimately reduce risk for cognitive decline and conditions like Alzheimer's disease in HF.

How Treatable is Vascular Dementia?

Vascular dementia is an umbrella term, encompassing the pathological changes in the brain due to cerebrovascular disease that result in dementia. Vascular dementia is the second most common form of dementia, after Alzheimer's disease. In this paper, I outline the concept of vascular dementia, the key aspects of the disease that are yet to be clarified, and the current status of clinical trials. Assessing these factors, I discuss how treatable vascular dementia presently is. Use of the term'vascular dementia'is riddled with uncertainties regarding disease classification, and non-standardized diagnostic criteria. There are difficulties in determining the exact relationship between cerebrovascular pathology and cognitive impairment. The comorbid effects of Alzheimer's pathology in some individuals also present an obstacle to reliable clinical diagnosis, and hinder research into effective management approaches. Vascular dementia is preventable and treatable, as there are established primary and secondary prevention measures for the causative cerebrovascular diseases, such as vascular risk factor intervention, antiplatelet therapy, and anticoagulation, amongst others. However, unlike Alzheimer's disease, there are no established symptomatic treatments for vascular dementia. Clinical trials of cholinesterase inhibitors and memantine indicate that they produce small cognitive benefits in patients with vascular dementia, though the exact clinical significance of these is uncertain. Data are insufficient to support the widespread use of these drugs in vascular dementia. Rehabilitation and physical and cognitive exercise may be beneficial, but evidence of cognitive benefit and relief of neuropsychiatric symptoms due to exercise is lacking.

Vitamin E and Alzheimer's Disease

It has been suggested that oxidative stress may contribute to the pathogenesis of Alzheimer's disease. Vitamin E is a potent antioxidant, and the results of some epidemiological studies have suggested that high intake of vitamin E through food is inversely associated with the incidence of Alzheimer's disease. Randomized controlled studies have shown that treatment with vitamin E could delay functional decline in patients with mild to moderate Alzheimer's disease. However, vitamin E had no cognitive benefits in patients with mild cognitive impairment or in generally healthy older women. Well-designed clinical trials or preventive interventions with vitamin E are necessary to establish its efficacy as therapeutic or preventive agents for Alzheimer's disease.

Could fingolimod provide cognitive benefits in patients with Huntington disease?

Neurodegenerative disease: Could fingolimod provide cognitive benefits in patients with Huntington disease?

Cardiac rehabilitation is associated with lasting improvements in cognitive function in older adults with heart failure

Objective Heart failure (HF) is a known risk factor for cognitive impairment. Cardiac rehabilitation (CR) may attenuate poor neurocognitive outcomes in HF via improved physical fitness—a significant promoter of cognitive function. However, no study has examined the possible acute and lasting benefits of CR on cognitive function in persons with HF.Methods and results Fifty-two patients with HF completed a 12-week Phase II CR program. All participants were administered neuropsychological testing and completed a brief physical fitness assessment at baseline, completion of CR (i.e. 12 weeks), and 12-month follow-up. Repeated measures analyses showed a significant time effect for both attention/executive function and memory (P 0.05). Attention/executive function performance increased from baseline to 12 weeks and these gains remained up to 12 months; memory was unchanged from baseline to 12 weeks, but then improved between the 12-week and 12-month time points. Physical fitness improved from baseline to 12 weeks and these benefits were maintained 12 months later. Changes in physical fitness and cognitive function over time did not reach a statistically significant association, though poorer physical fitness was associated with decreased cognitive performance at the baseline and 12-month time points.Conclusions CR is associated with both acute and lasting cognitive benefits in patients with HF. Prospective studies with extended follow-ups are needed to clarify the mechanisms that underpin cognitive improvements following CR (e.g., improved cerebral perfusion) and whether CR can ultimately reduce risk for cognitive decline and conditions like Alzheimer’s disease in HF.

Souvenaid®: a new approach to management of early Alzheimer's disease.

Synaptic loss correlates closely with cognitive deficits in Alzheimer's disease and represents a new target for intervention. Souvenaid® is the first medical nutrition product to be designed to support synapse formation and function in early Alzheimer's disease, and has undergone an extensive, 12-year development programme. The relatively large amount of clinical data available for Souvenaid® is unusual for a medical nutrition product. Souvenaid® contains omega-3 polyunsaturated fatty acids (docosahexaenoic acid and eicosapentaenoic acid), uridine (as uridine monophosphate) and choline which are nutritional precursors required for synaptic membrane phospholipid synthesis, together with phospholipids and other cofactors. Souvenaid® has demonstrated cognitive benefits in patients with mild Alzheimer's disease but not in patients with mild-to-moderate Alzheimer's disease. Two randomised, double-blind, controlled trials (duration 12 and 24 weeks) in patients with mild Alzheimer's disease untreated with acetylcholinesterase inhibitors and/or memantine have demonstrated that Souvenaid® is well tolerated and improves episodic memory performance. The daily intake of Souvenaid® has not been associated with any harmful effects or interactions with medications and none are anticipated. The ongoing, 24-month, European Union-funded LipiDiDiet trial in subjects with prodromal Alzheimer's disease is evaluating the potential benefits of Souvenaid® on memory and in slowing progression to Alzheimer's dementia. If Souvenaid® induces synaptogenesis and improved synaptic function, it may provide benefits in other clinical conditions characterised by neurodegeneration. A number of trials are ongoing and planned to evaluate the potential wider benefits of Souvenaid®.

Improvement of Cognitive Deficit in Alzheimer's Disease Patients by Long Term Treatment with Korean Red Ginseng

A 24-week randomized open-label study with Korean red ginseng (KRG) showed cognitive benefits in patients with Alzheimer’s disease. To further determine long-term effect of KRG, the subjects were recruited to be followed up to 2 yr. Cognitive function was evaluated every 12 wk using the Alzheimer’s Disease Assessment Scale (ADAS) and the Korean version of the Mini Mental Status Examination (K-MMSE) with the maintaining dose of 4.5 g or 9.0 g KRG per d. At 24 wk, there had been a significant improvement in KRG-treated groups. In the long-term evaluation of the efficacy of KRG after 24 wk, the improved MMSE score remained without significant decline at the 48th and 96th wk. ADAS-cog showed similar findings. Maximum improvement was found around week 24. In conclusion, the effect of KRG on cognitive functions was sustained for 2 yr follow-up, indicating feasible efficacies of long-term follow-up for Alzheimer’s disease.

Effects of a 6-Month Cognitive Intervention Program on Brain Metabolism in Amnestic Mild Cognitive Impairment and Mild Alzheimer's Disease

The effect of cognitive intervention on brain metabolism in Alzheimer's disease (AD) is largely unexplored. Therefore, we aimed to investigate clinical cognitive parameters and 18FDG PET to test for effects of a cognitive intervention in patients with amnestic mild cognitive impairment (aMCI) or mild AD. Patients with aMCI (n = 24) or mild AD (n = 15) were randomly assigned either to cognitive intervention groups (IGs), receiving weekly sessions of group-based multicomponent cognitive intervention, or active control groups (CGs), receiving pencil-paper exercises for self-study. We obtained resting-state FDG-PET scans and neuropsychological testing at baseline and after six-months. Normalized FDG-PET images were analyzed using voxel-based SPM5 approaches to determine longitudinal changes, group-by-time interactions, and correlations with neuropsychological outcome parameters. Primary global cognitive outcome was determined by analyses of covariance with MMSE and ADAS-cog scores as dependent measures. Both, aMCI and AD subgroups of CGs showed widespread bilateral cortical declines in FDG uptake, while the AD subgroup of IGs showed discrete decline or rather no decline in case of the aMCI subgroup. Group by time analyses revealed strongest attenuation of metabolic decline in the aMCI subgroup of the IGs, involving left superior temporal- and anterior cingulate gyrus. However, correlation analyses revealed only weak non-significant associations between increased FDG uptake and improvement in primary or secondary outcome parameters. Concurrently, there was significant improvement in global cognitive status in the aMCI subgroup of the IGs. A six-month cognitive intervention imparted cognitive benefits in patients with aMCI, which were concurrent with an attenuated decline of glucose metabolism in cortical regions affected by neurodegenerative AD.

Effect of Donepezil on Cognition in Severe Alzheimer's Disease: A Pooled Data Analysis

To better characterize response to donepezil in patients with severe AD, Severe Impairment Battery (SIB) data were pooled from four donepezil clinical trials (N=904). Changes in SIB total and domain scores from baseline to week 24 were compared between placebo and donepezil treatment groups (observed case analysis). Analyses were stratified by baseline severity (Mini-Mental State Examination [MMSE] scores 1-5, 6-9, 10-12 and 13-17) to allow investigation of responses at different stages of cognitive impairment. Relationships to global and functional measures were explored. The difference between donepezil- and placebo-treated patients in least squares (LS) mean change in SIB total scores from baseline to week 24 was 6.22 (p < 0.0001, Cohen's d, 0.53). Treatment-placebo differences were statistically significant for each baseline severity stratum, being greatest for the MMSE 6-9 stratum (LS mean difference, 7.60; p < 0.0001, Cohen's d, 0.66). Treatment-placebo differences in LS mean change in SIB domain scores significantly favored donepezil for seven of nine domains (range, p = 0.0056 to p < 0.0001; Cohen's d, 0.17-0.48). Change in total SIB score correlated significantly with change in measures of activities of daily living and global status. These results indicate that donepezil provides cognitive benefits in patients with severe AD, including those most markedly impaired. The treatment effect size and correlation between improvements in SIB scores and functional and global outcome measures suggest the drug-placebo differences are clinically meaningful.

¿Es factible la vacunación contra la encefalopatía espongiforme transmisible?

Prion diseases are a unique category of illness, affecting both animals and humans, where the underlying pathogenesis is related to a conformation change of the cellular form of a normal, self-protein called a prion protein (PrP(c) [C for cellular]) to a pathological and infectious conformation known as scrapie form (PrPsc [Sc for scrapie]). Currently, all prion diseases are without effective treatment and are universally fatal. The emergence of bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease has highlighted the need to develop possible therapies. In Alzheimer's disease (AD), which has similarities to prion diseases, both passive and active immunisation have been shown to be highly effective at preventing disease and cognitive deficits in model animals. In a human trial of active vaccination in AD, despite indications of cognitive benefits in patients with an adequate humoral response, 6% of patients developed significant complications related to excessive cell-mediated immunity. This experience highlights that immunotherapies designed to be directed against a self-antigen have to finely balance an effective humoral immune response with potential autoimmune toxicity. Many prion diseases have the gut as a portal of infectious agent entry. This makes mucosal immunisation a potentially very attractive method to partially or completely prevent prion entry across the gut barrier and to also produce a modulated immune response that is unlikely to be associated with any toxicity. The authors' recent results using an attenuated Salmonella vaccine strain expressing the prion protein show that mucosal vaccination can partially protect against prion infection from a peripheral source, suggesting the feasibility of this approach.

Galantamine shows sustained cognitive benefits in patients with Alzheimer's disease (AD),

Galantamine shows sustained cognitive benefits in patients with Alzheimer's disease (AD),