The Impact of Symptom Severity on the Cost of Alzheimer's Disease

2002 ◽  
Vol 50 (2) ◽  
pp. 321-327 ◽  
Author(s):  
Gary W. Small ◽  
Diana D. McDonnell ◽  
Rachelle L. Brooks ◽  
George Papadopoulos
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Symptom Severity ◽  
The Cost ◽  
The Impact

scholarly journals 401 - The Costs of Agitation: A Literature Review

2020 ◽  
Vol 32 (S1) ◽  
pp. 117-117
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Literature Review ◽  
Service Use ◽  
Neuropsychiatric Symptoms ◽  
Unmet Need ◽  
Cochrane Library ◽  
Future Research ◽  
The Cost ◽  
The Impact

PRESENTING AUTHOR:Mary Michael, Vice President, Patient Advocacy and Stakeholder Management, Otsuka America Pharmaceutical, Inc.OBJECTIVE:To evaluate the extent to which the cost of both treated and untreated agitation in Alzheimer’s disease has been studied in order to inform future research and development of predictive models of the cost of untreated agitation in Alzheimer’s disease.BACKGROUND:There is inadequate understanding of the costs of agitation in Alzheimer’s disease in the scientific and academic literature. Agitation in Alzheimer’s disease contributes to negative social and financial outcomes for people with the condition, their care partners, and health systems. When left untreated, the impact of these outcomes is exacerbated, yet the scale of this impact is unknown. This gap in the literature both reflects and perpetuates the broader under-recognition of agitation as a serious unmet need in the Alzheimer’s community. Conversely, a better understanding of the costs can help elevate agitation within the global Alzheimer’s dialogue.METHODS:We used MEDLINE, PubMed, PsychINFO the Cochrane Library and Google Scholar databases to identify relevant articles published between 2000 until May 2020. We also reviewed reliable literature published outside of these databases. Keywords utilized in the search include agitation in Alzheimer’s, neuropsychiatric symptoms of Alzheimer’s, cost of informal and formal care, Medicare and Medicaid costs, economic costs associated to delirium, among others. Only articles in English were included. Inclusion and exclusion criteria were determined by study design, data source and population studied, number of cases included in analysis, source of health service use or cost data, statistical methods and agitation in Alzheimer’s attributable and/or incremental costs.RESULTS:Results will describe the breadth and depth to which costs of treated and untreated agitation in Alzheimer’s have been examined, indicating data and statistical methodology used.CONCLUSIONS:This literature review serves as the basis for understanding global costs of agitation in Alzheimer’s disease. From our analysis, we recommend that further cost modeling activities be conducted. We also urge the greater community to use these findings to elevate agitation to the top of the Alzheimer’s agenda.

scholarly journals Accuracy-time optimisation with cost-sensitive feature selection for Alzheimer's disease diagnosis

2021 ◽  
Author(s):  
Niamh McCombe ◽  
Xuemei Ding ◽  
Girijesh Prasad ◽  
Paddy Gillespie ◽  
David P Finn ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Feature Selection ◽  
Diagnostic Accuracy ◽  
Disease Diagnosis ◽  
Machine Learning Techniques ◽  
Assessment Time ◽  
Alzheimer’S Disease Diagnosis ◽  
The Cost ◽  
The Impact

Objective: Despite the potential of machine learning techniques to improve dementia diagnostic processes, research outcomes are often not readily translated to or adopted in clinical practice. Importantly, the cost of assessment items, in terms of assessment time, has yet to be taken into account in feature-selection based optimisation for dementia diagnosis. We address these issues by considering the impact of assessment time as a practical constraint for feature selection of cognitive and functional assessments in Alzheimer's disease diagnosis. Methods: We use three different feature selection algorithms to select informative subsets of dementia assessment items from a large open source dementia dataset. We use cost cost-sensitive feature selection to optimise our feature selection results for assessment time as well as accuracy. To encourage the clinical adoption and further evaluation of our proposed accuracy-vs-time optimisation algorithms, we also implement a sandbox-like toolbox with graphical user interface to evaluate user-chosen subsets of assessment items. Results: We find that there are subsets of accuracy-time optimised assessment items that can perform better in terms of diagnostic accuracy and/or total assessment time than most other standard assessments. Discussion: Overall, the cost-benefit optimisation analysis and accompanying sandbox tool can facilitate clinical users and other stakeholders to apply their own domain knowledge to analyse and decide which dementia diagnostic assessment items are useful, and aid the redesigning of dementia diagnostic assessments. Clinical Impact (Clinical Research): By optimising diagnostic accuracy and assessment time, we redesign predictive and efficient dementia diagnostic assessments and develop a sandbox interface to facilitate evaluation and testing by clinicians and non-specialists.

The cost-utility of the rivastigmine transdermal patch in the management of patients with moderate Alzheimer's disease in the US

2009 ◽  
Vol 36 (S 02) ◽  
Author(s):  
A Brennan ◽  
B Nagy ◽  
A Brandtmüller ◽  
SK Thomas ◽  
M Gallagher ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cost Utility ◽  
Transdermal Patch ◽  
The Us ◽  
The Cost

Fluoxetine Protects against Dendritic Spine Loss in Middle-aged APPswe/PSEN1dE9 Double Transgenic Alzheimer’s Disease Mice

2020 ◽  
Vol 17 (1) ◽  
pp. 93-103 ◽  
Author(s):  
Jing Ma ◽  
Yuan Gao ◽  
Wei Tang ◽  
Wei Huang ◽  
Yong Tang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dendritic Spines ◽  
Dendritic Spine ◽  
Early Stage ◽  
Learning Ability ◽  
Middle Aged ◽  
Protein Levels ◽  
Spine Pathology ◽  
The Impact

Background: Studies have suggested that cognitive impairment in Alzheimer’s disease (AD) is associated with dendritic spine loss, especially in the hippocampus. Fluoxetine (FLX) has been shown to improve cognition in the early stage of AD and to be associated with diminishing synapse degeneration in the hippocampus. However, little is known about whether FLX affects the pathogenesis of AD in the middle-tolate stage and whether its effects are correlated with the amelioration of hippocampal dendritic dysfunction. Previously, it has been observed that FLX improves the spatial learning ability of middleaged APP/PS1 mice. Objective: In the present study, we further characterized the impact of FLX on dendritic spines in the hippocampus of middle-aged APP/PS1 mice. Results: It has been found that the numbers of dendritic spines in dentate gyrus (DG), CA1 and CA2/3 of hippocampus were significantly increased by FLX. Meanwhile, FLX effectively attenuated hyperphosphorylation of tau at Ser396 and elevated protein levels of postsynaptic density 95 (PSD-95) and synapsin-1 (SYN-1) in the hippocampus. Conclusion: These results indicated that the enhanced learning ability observed in FLX-treated middle-aged APP/PS1 mice might be associated with remarkable mitigation of hippocampal dendritic spine pathology by FLX and suggested that FLX might be explored as a new strategy for therapy of AD in the middle-to-late stage.

Emerging Proof of Protein Misfolding and Interactions in Multifactorial Alzheimer's Disease

2020 ◽  
Vol 20 (26) ◽  
pp. 2380-2390 ◽  
Author(s):  
Md. Sahab Uddin ◽  
Abdullah Al Mamun ◽  
Md. Ataur Rahman ◽  
Tapan Behl ◽  
Asma Perveen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Misfolding ◽  
Neurodegenerative Disorder ◽  
Senile Plaques ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Misfolded Proteins ◽  
Cell Organelles ◽  
The Impact

Objective: Alzheimer's disease (AD) is a devastating neurodegenerative disorder, characterized by the extracellular accumulations of amyloid beta (Aβ) as senile plaques and intracellular aggregations of tau in the form of neurofibrillary tangles (NFTs) in specific brain regions. In this review, we focus on the interaction of Aβ and tau with cytosolic proteins and several cell organelles as well as associated neurotoxicity in AD. Summary: Misfolded proteins present in cells accompanied by correctly folded, intermediately folded, as well as unfolded species. Misfolded proteins can be degraded or refolded properly with the aid of chaperone proteins, which are playing a pivotal role in protein folding, trafficking as well as intermediate stabilization in healthy cells. The continuous aggregation of misfolded proteins in the absence of their proper clearance could result in amyloid disease including AD. The neuropathological changes of AD brain include the atypical cellular accumulation of misfolded proteins as well as the loss of neurons and synapses in the cerebral cortex and certain subcortical regions. The mechanism of neurodegeneration in AD that leads to severe neuronal cell death and memory dysfunctions is not completely understood until now. Conclusion: Examining the impact, as well as the consequences of protein misfolding, could help to uncover the molecular etiologies behind the complicated AD pathogenesis.

scholarly journals Metabolic phenotyping reveals a reduction in the bioavailability of serotonin and kynurenine pathway metabolites in both the urine and serum of individuals living with Alzheimer’s disease

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Luke Whiley ◽  
◽  
Katie E. Chappell ◽  
Ellie D’Hondt ◽  
Matthew R. Lewis ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Systemic Inflammation ◽  
Metabolic Phenotyping ◽  
Acid Urine ◽  
Metabolite Concentrations ◽  
Ssri Medication ◽  
The Impact ◽  
Urine And Serum ◽  
Urine Serum

Abstract Background Both serotonergic signalling disruption and systemic inflammation have been associated with the pathogenesis of Alzheimer’s disease (AD). The common denominator linking the two is the catabolism of the essential amino acid, tryptophan. Metabolism via tryptophan hydroxylase results in serotonin synthesis, whilst metabolism via indoleamine 2,3-dioxygenase (IDO) results in kynurenine and its downstream derivatives. IDO is reported to be activated in times of host systemic inflammation and therefore is thought to influence both pathways. To investigate metabolic alterations in AD, a large-scale metabolic phenotyping study was conducted on both urine and serum samples collected from a multi-centre clinical cohort, consisting of individuals clinically diagnosed with AD, mild cognitive impairment (MCI) and age-matched controls. Methods Metabolic phenotyping was applied to both urine (n = 560) and serum (n = 354) from the European-wide AddNeuroMed/Dementia Case Register (DCR) biobank repositories. Metabolite data were subsequently interrogated for inter-group differences; influence of gender and age; comparisons between two subgroups of MCI - versus those who remained cognitively stable at follow-up visits (sMCI); and those who underwent further cognitive decline (cMCI); and the impact of selective serotonin reuptake inhibitor (SSRI) medication on metabolite concentrations. Results Results revealed significantly lower metabolite concentrations of tryptophan pathway metabolites in the AD group: serotonin (urine, serum), 5-hydroxyindoleacetic acid (urine), kynurenine (serum), kynurenic acid (urine), tryptophan (urine, serum), xanthurenic acid (urine, serum), and kynurenine/tryptophan ratio (urine). For each listed metabolite, a decreasing trend in concentrations was observed in-line with clinical diagnosis: control > MCI > AD. There were no significant differences in the two MCI subgroups whilst SSRI medication status influenced observations in serum, but not urine. Conclusions Urine and serum serotonin concentrations were found to be significantly lower in AD compared with controls, suggesting the bioavailability of the neurotransmitter may be altered in the disease. A significant increase in the kynurenine/tryptophan ratio suggests that this may be a result of a shift to the kynurenine metabolic route due to increased IDO activity, potentially as a result of systemic inflammation. Modulation of the pathways could help improve serotonin bioavailability and signalling in AD patients.

scholarly journals Shotgun lipidomics of liver and brain tissue of Alzheimer’s disease model mice treated with acitretin

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Anna A. Lauer ◽  
Daniel Janitschke ◽  
Malena dos Santos Guilherme ◽  
Vu Thu Thuy Nguyen ◽  
Cornel M. Bachmann ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
Amyloid Β ◽  
Lipid Homeostasis ◽  
Medical Surveillance ◽  
Shotgun Lipidomics ◽  
App Processing ◽  
Cognitive Improvement ◽  
The Impact

AbstractAlzheimer’s disease (AD) is a very frequent neurodegenerative disorder characterized by an accumulation of amyloid-β (Aβ). Acitretin, a retinoid-derivative and approved treatment for Psoriasis vulgaris, increases non-amyloidogenic Amyloid-Precursor-Protein-(APP)-processing, prevents Aβ-production and elicits cognitive improvement in AD mouse models. As an unintended side effect, acitretin could result in hyperlipidemia. Here, we analyzed the impact of acitretin on the lipidome in brain and liver tissue in the 5xFAD mouse-model. In line with literature, triglycerides were increased in liver accompanied by increased PCaa, plasmalogens and acyl-carnitines, whereas SM-species were decreased. In brain, these effects were partially enhanced or similar but also inverted. While for SM and plasmalogens similar effects were found, PCaa, TAG and acyl-carnitines showed an inverse effect in both tissues. Our findings emphasize, that potential pharmaceuticals to treat AD should be carefully monitored with respect to lipid-homeostasis because APP-processing itself modulates lipid-metabolism and medication might result in further and unexpected changes. Moreover, deducing effects of brain lipid-homeostasis from results obtained for other tissues should be considered cautiously. With respect to acitretin, the increase in brain plasmalogens might display a further positive probability in AD-treatment, while other results, such as decreased SM, indicate the need of medical surveillance for treated patients.

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