Jpad-Journal of Prevention of Alzheimers Disease最新文献

{"title":"Randomized, Placebo Controlled Trial of NPT088, A Phage-Derived, Amyloid-Targeted Treatment for Alzheimer’s Disease","authors":"D. Michelson, M. Grundman, K. Magnuson, R. Fisher, Jonathan M. Levenson, Paul S. Aisen, K. Marek, Martha Gray, Franz Hefti","doi":"10.14283/jpad.2019.37","DOIUrl":"https://doi.org/10.14283/jpad.2019.37","url":null,"abstract":"The engineered fusion protein NPT088 targets amyloid in vitro and in animal models of Alzheimer’s disease. Previous studies showed that NPT088 treatment reduced β-amyloid plaque and tau aggregate loads in mouse disease models. Here, we present the results from an initial clinical study of NPT088 in patients with mild to moderate Alzheimer’s disease. Patients were treated with 4 dose levels of NPT088 for 6 months to evaluate its safety and tolerability. Exploratory measurements included measurement of change in β-amyloid plaque and tau burden utilizing Positron Emission Tomography imaging as well as measures of Alzheimer’s disease symptoms. At endpoint NPT088 was generally safe and well-tolerated with the most prominent finding being infusion reactions in a minority of patients. No effect of NPT088 on brain plaques, tau aggregates or Alzheimer’s disease symptoms was observed.","PeriodicalId":48606,"journal":{"name":"Jpad-Journal of Prevention of Alzheimers Disease","volume":"109 1","pages":"228 - 231"},"PeriodicalIF":6.4,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14283/jpad.2019.37","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66893456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application of the NIA-AA Research Framework: Towards a Biological Definition of Alzheimer’s Disease using Cerebrospinal Fluid Biomarkers in the AIBL Study","authors":"S. Burnham, Preciosa M. Coloma, Qiao-Xin Li, Steven J. Collins, G. Savage, Simon M. Laws, Simon M. Laws, J. Doecke, P. Maruff, R. Martins, R. Martins, D. Ames, Christopher Rowe, Colin L. Masters, V. Villemagne","doi":"10.14283/jpad.2019.25","DOIUrl":"https://doi.org/10.14283/jpad.2019.25","url":null,"abstract":"BackgroundThe National Institute on Aging and Alzheimer’s Association (NIA-AA) have proposed a new Research Framework: Towards a biological definition of Alzheimer’s disease, which uses a three-biomarker construct: Aß-amyloid, tau and neurodegeneration AT(N), to generate a biomarker based definition of Alzheimer’s disease.ObjectivesTo stratify AIBL participants using the new NIA-AA Research Framework using cerebrospinal fluid (CSF) biomarkers. To evaluate the clinical and cognitive profiles of the different groups resultant from the AT(N) stratification. To compare the findings to those that result from stratification using two-biomarker construct criteria (AT and/or A(N)).DesignIndividuals were classified as being positive or negative for each of the A, T, and (N) categories and then assigned to the appropriate AT(N) combinatorial group: A−T−(N)−; A+T-(N)−; A+T+(N)−; A+T−(N)+; A+T+(N)+; A−T+(N)−; A−T−(N)+; A−T+(N)+. In line with the NIA-AA research framework, these eight AT(N) groups were then collapsed into four main groups of interest (normal AD biomarkers, AD pathologic change, AD and non-AD pathologic change) and the respective clinical and cognitive trajectories over 4.5 years for each group were assessed. In two sensitivity analyses the methods were replicated after assigning individuals to four groups based on being positive or negative for AT biomarkers as well as A(N) biomarkers.SettingTwo study centers in Melbourne (Victoria) and Perth (Western Australia), Australia recruited MCI individuals and individuals with AD from primary care physicians or tertiary memory disorder clinics. Cognitively healthy, elderly NCs were recruited through advertisement or via spouses of participants in the study.ParticipantsOne-hundred and forty NC, 33 MCI participants, and 27 participants with AD from the AIBL study who had undergone CSF evaluation using Elecsys® assays.Intervention (if any)Not applicable.MeasurementsThree CSF biomarkers, namely amyloid β1–42, phosphorylated tau181, and total tau, were measured to provide the AT(N) classifications. Clinical and cognitive trajectories were evaluated using the AIBL Preclinical Alzheimer Cognitive Composite (AIBL-PACC), a verbal episodic memory composite, an executive function composite, California Verbal Learning Test–Second Edition; Long-Delay Free Recall, Mini-Mental State Examination, and Clinical Dementia Rating Sum of Boxes scores.ResultsThirty-eight percent of the elderly NCs had no evidence of abnormal AD biomarkers, whereas 33% had biomarker levels consistent with AD or AD pathologic change, and 29% had evidence of non-AD biomarker change. Among NC participants, those with biomarker evidence of AD pathology tended to perform worse on cognitive outcome assessments than other biomarker groups. Approximately three in four participants with MCI or AD had biomarker levels consistent with the research framework’s definition of AD or AD pathologic change. For MCI participants, a decrease in AIBL-PACC score","PeriodicalId":48606,"journal":{"name":"Jpad-Journal of Prevention of Alzheimers Disease","volume":"1 1","pages":"1-8"},"PeriodicalIF":6.4,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14283/jpad.2019.25","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66893085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mediterranean-Dash Intervention for Neurodegenerative Delay (MIND) Diet Slows Cognitive Decline After Stroke.","authors":"L Cherian, Y Wang, K Fakuda, S Leurgans, N Aggarwal, M Morris","doi":"10.14283/jpad.2019.28","DOIUrl":"10.14283/jpad.2019.28","url":null,"abstract":"<p><strong>Objective: </strong>This study sought to determine if the MIND diet (a hybrid of the Mediterranean and Dash diets, with modifications based on the science of nutrition and the brain), is effective in preventing cognitive decline after stroke.</p><p><strong>Design: </strong>We analyzed 106 participants of a community cohort study who had completed a diet assessment and two or more annual cognitive assessments and who also had a clinical history of stroke. Cognition in five cognitive domains was assessed using structured clinical evaluations that included a battery of 19 cognitive tests. MIND diet scores were computed using a valid food frequency questionnaire (FFQ). Dietary components of the MIND diet included whole grains, leafy greens and other vegetables, berries, beans, nuts, lean meats, fish, poultry, and olive oil and reduced consumption of cheese, butter, fried foods, and sweets. MIND diet scores were modeled in tertiles. The influence of baseline MIND score on change in a global cognitive function measure and in the five cognitive domains was assessed using linear mixed models adjusted for age and other potential confounders.</p><p><strong>Results: </strong>With adjustment for age, sex, education, APOE-ε4, caloric intake, smoking, and participation in cognitive and physical activities, the top vs lowest tertiles of MIND diet scores had a slower rate of global cognitive decline (β = .08; CI = 0.0074, 0.156) over an average of 5.9 years of follow-up.</p><p><strong>Conclusions: </strong>High adherence to the MIND diet was associated with a slower rate of cognitive decline after stroke.</p>","PeriodicalId":48606,"journal":{"name":"Jpad-Journal of Prevention of Alzheimers Disease","volume":"1 1","pages":"267-273"},"PeriodicalIF":6.4,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7199507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66893394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Can Digital Technology Advance the Development of Treatments for Alzheimer’s Disease?","authors":"M. Mc Carthy, P. Schueler","doi":"10.14283/jpad.2019.32","DOIUrl":"https://doi.org/10.14283/jpad.2019.32","url":null,"abstract":"The report explores the potential digital technology has to generate novel endpoints and digital biomarkers for Alzheimer’s disease drug development studies. Drawing from literature and novel pilots, we explore the value of innovative digital technology to digitize physiological behaviours such as sleep disturbance and gait changes. Technology now exists to monitor and quantify our use and interaction with electronics in the home, the use of social platforms and smart-phones, geolocation, sleep and activity patterns. These multimodal digital data are a feasible alternative to capturing the more complex activities of daily living that require higher cognitive processes and are a sensitive predictor of disease. The combination of biosensors and the internet of things (IoT), offers the potential to collect highly relevant, objective data in a continuous, passive and low burden manner. Digital endpoints and biomarkers could have value in the diagnosis, monitoring and development of therapies for patients living with Alzheimer’s disease.","PeriodicalId":48606,"journal":{"name":"Jpad-Journal of Prevention of Alzheimers Disease","volume":"6 1","pages":"217 - 220"},"PeriodicalIF":6.4,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66893242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Financial Management Skills in Aging, MCI and Dementia: Cross Sectional Relationship to 18F-Florbetapir PET Cortical β-amyloid Deposition","authors":"Sierra Tolbert, Sierra Tolbert, Y. Liu, C. Hellegers, J. Petrella, Michael W. Weiner, T. Wong, P. Doraiswamy","doi":"10.14283/jpad.2019.26","DOIUrl":"https://doi.org/10.14283/jpad.2019.26","url":null,"abstract":"BackgroundThere is a need to more fully characterize financial capacity losses in the preclinical and prodromal stages of Alzheimer’s disease (AD) and their pathological substrates.ObjectivesTo test the association between financial skills and cortical β-amyloid deposition in aging and subjects at risk for AD.DesignCross-sectional analyses of data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI-3) study conducted across 50 plus sites in the US and Canada.SettingMulticenter biomarker study.Participants243 subjects (144 cognitively normal, 79 mild cognitive impairment [MCI], 20 mild AD).Measurements18F-Florbetapir brain PET scans to measure global cortical β-amyloid deposition (SUVr) and the Financial Capacity Instrument Short Form (FCI-SF) to evaluate an individual’s financial skills in monetary calculation, financial concepts, checkbook/register usage, and bank statement usage. There are five sub scores and a total score (range of 0–74) with higher scores indicating better financial skill.ResultsFCI-SF total score was significantly worse in MCI [Cohen’s d= 0.9 (95%CI: 0.6–1.2)] and AD subjects [Cohen’s d=3.1(CI: 2.5–3.7)] compared to normals. Domain scores and completion times also showed significant difference. Across all subjects, higher cortical β-amyloid SUVr was significantly associated with worse FCI-SF total score after co-varying for age, education, and cognitive score [Cohen’s f2=0.751(CI: 0.5–1.1)]. In cognitively normal subjects, after covarying for age, gender, and education, higher β -amyloid PET SUVr was associated with longer task completion time [Cohen’s f2=0.198(CI: 0.06–0.37)].ConclusionUsing a multicenter study sample, we document that financial capacity is impaired in the prodromal and mild stages of AD and that such impairments are, in part, associated with the extent of cortical β-amyloid deposition. In normal aging, β-amyloid deposition is associated with slowing of financial tasks. These data confirm and extend prior research highlighting the utility of financial capacity assessments in at risk samples.","PeriodicalId":48606,"journal":{"name":"Jpad-Journal of Prevention of Alzheimers Disease","volume":"1 1","pages":"1-9"},"PeriodicalIF":6.4,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14283/jpad.2019.26","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66893162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparing the Standard and Electronic Versions of the Alzheimer’s Disease Assessment Scale — Cognitive Subscale: A Validation Study","authors":"Todd M. Solomon, J. Barbone, H. T. Feaster, David S. Miller, Guy B. deBros, Cynthia A. Murphy, D. Michalczuk","doi":"10.14283/jpad.2019.27","DOIUrl":"https://doi.org/10.14283/jpad.2019.27","url":null,"abstract":"The Alzheimer’s Disease Assessment Scale (ADAS-Cog) has become the de facto gold-standard for assessing the efficacy of putative anti-dementia treatments. There has been an increasing interest in providing greater standardization, automation, and administration consistency to the scale. Recently, electronic versions of the ADAS-Cog (eADAS-Cog) have been utilized in clinical trials and demonstrated significant reductions in frequency of rater error as compared to paper. In order to establish validity of the electronic version (eADAS-Cog), 20 subjects who had received a diagnosis of probable Alzheimer’s disease (AD) at a private US Memory Clinic completed a single-center, randomized, counterbalanced, prospective trial comparing a version of the eADAS-Cog to the standard paper scale. Interclass Correlation Coefficient on total scores and Kappa analysis on domain scores yielded high agreement (0.88–0.99). Effects of order and mode of administration on ADAS-Cog total scores did not demonstrate a significant main effect. Overall, this study establishes adequate concurrent validity between the ADAS-Cog and eADAS-Cog among an adult population with diagnosed AD.","PeriodicalId":48606,"journal":{"name":"Jpad-Journal of Prevention of Alzheimers Disease","volume":"43 1","pages":"1-5"},"PeriodicalIF":6.4,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14283/jpad.2019.27","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66893284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropsychological, Psychiatric, and Functional Correlates of Clinical Trial Enrollment","authors":"D. Hammers, Norman L. Foster, J. Hoffman, T. Greene, Kevin Duff","doi":"10.14283/jpad.2019.38","DOIUrl":"https://doi.org/10.14283/jpad.2019.38","url":null,"abstract":"Screen failure rates in Alzheimer’s disease (AD) clinical trial research are unsustainable, with participant recruitment being a top barrier to AD research progress. The purpose of this project was to understand the neuropsychological, psychiatric, and functional features of individuals who failed screening measures for AD trials. Previously collected clinical data from 38 patients (aged 50–83) screened for a specific industry-sponsored clinical trial of MCI/early AD (Biogen 221AD302, [EMERGE]) were analyzed to identify predictors of AD trial screen pass/fail status. Worse performance on non-memory cognitive domains like crystalized knowledge, executive functioning, and attention, and higher self-reported anxiety, was associated with failing the screening visit for the EMERGE AD clinical trial, whereas we were not able to detect a relationship between screening status and memory performance, self-reported depression, or self-reported daily functioning. By identifying predictors of AD trial screen passing/failure, this research may influence decision-making about which patients are most likely to successfully enroll in a trial, thereby potentially lowering participant burden, maximizing study resources, and reducing costs.","PeriodicalId":48606,"journal":{"name":"Jpad-Journal of Prevention of Alzheimers Disease","volume":"6 1","pages":"242 - 247"},"PeriodicalIF":6.4,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14283/jpad.2019.38","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66893480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prospective Evaluation of Cognitive Health and Related Factors in Elderly at Risk for Developing Alzheimer’s Dementia: A Longitudinal Cohort Study","authors":"C. Udeh-Momoh, G. Price, M. Ropacki, N. Ketter, T. Andrews, H. Arrighi, H. Brashear, Catherine E. Robb, Darina T Bassil, M. Cohn, L. Curry, B. Su, D. Perera, P. Giannakopoulou, J. Car, Heather A. Ward, R. Perneczky, R. Perneczky, R. Perneczky, G. Novak, L. Middleton","doi":"10.14283/jpad.2019.31","DOIUrl":"https://doi.org/10.14283/jpad.2019.31","url":null,"abstract":"BackgroundThe CHARIOT PRO Main study is a prospective, non-interventional study evaluating cognitive trajectories in participants at the preclinical stage of Alzheimer’s disease (AD) classified by risk levels for developing mild cognitive impairment due to AD (MCI-AD).ObjectivesThe study aimed to characterize factors and markers influencing cognitive and functional progression among individuals at-risk for developing MCI-AD, and examine data for more precise predictors of cognitive change, particularly in relation to APOE ε4 subgroup.DesignThis single-site study was conducted at the Imperial College London (ICL) in the United Kingdom. Participants 60 to 85 years of age were classified as high, medium (amnestic or non-amnestic) or low risk for developing MCI-AD based on RBANS z-scores. A series of clinical outcome assessments (COAs) on factors influencing baseline cognitive changes were collected in each of the instrument categories of cognition, lifestyle exposure, mood, and sleep. Data collection was planned to occur every 6 months for 48 months, however the median follow-up time was 18.1 months due to early termination of study by the sponsor.Results987 participants were screened, among them 690 participants were actively followed-up post baseline, of whom 165 (23.9%) were APOE ε4 carriers; with at least one copy of the allele. The mean age was 68.73 years, 94.6% were white, 57.4% were female, and 34.8% had a Family History of Dementia with a somewhat larger percentage in the APOE ε4 carrier group (42.4%) compared to the non-carrier group (32.4%). Over half of the participants were married and 53% had a Bachelor’s or higher degree. Most frequently, safety events typical for this population consisted of upper respiratory tract infection (10.4%), falls (5.2%), hypertension (3.5%) and back pain (3.0%).Conclusion (clinical relevance)AD-related measures collected during the CHARIOT PRO Main study will allow identification and evaluation of AD risk factors and markers associated with cognitive performance from the pre-clinical stage. Evaluating the psycho-biological characteristics of these pre-symptomatic individuals in relation to their natural neurocognitive trajectories will enhance current understanding on determinants of the initial signs of cognitive changes linked to AD.","PeriodicalId":48606,"journal":{"name":"Jpad-Journal of Prevention of Alzheimers Disease","volume":"1 1","pages":"1-11"},"PeriodicalIF":6.4,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14283/jpad.2019.31","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66893113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Symposia","authors":"A. Lo, C. D. Evans, Michele Mancini, Qun-Fu Lin, Hong Wang, Peng Liu, Sergey, Shcherbinin, Ming Lu, Arnaud Charil, B. A. Willis, Michael, Irizarry, Robert Alexander, Daniel K. Burns, K. Welsh-Bohmer, Carl Chiang, Meredith Culp, J. O’neil, B.L. Plassman, Craig, Metz, Deborah Yarbrough, Jingtao Wu, R. Evans, Kumar Budur, Stephen K. Brannan, Ann M. Saunders, Emiliangelo Ratti","doi":"10.14283/jpad.2018.39","DOIUrl":"https://doi.org/10.14283/jpad.2018.39","url":null,"abstract":"Introduction: The amyloid hypothesis proposes that Aβ peptides are intimately involved in the etiology of Alzheimer’s disease (AD) via their aggregation to form toxic complexes that lead to neurodegeneration. Aβ is produced via sequential proteolytic cleavage of the parent molecule, amyloid precursor protein, by β-secretase (BACE1) followed by γ-secretase. Inhibition of BACE1 is a potential novel therapeutic strategy for slowing or halting progression of AD by reducing Aβ production. This approach differs from previous anti-amyloid approaches using monoclonal antibodies to clear Aβ. In the first large-scale clinical trial (EPOCH) of a BACE1 inhibitor, verubecestat doses of 12 mg and 40 mg were ineffective at slowing the rate of cognitive or functional decline over 78 weeks in participants with clinically diagnosed mild-to-moderate AD, despite reducing cerebrospinal fluid (CSF) Aβ levels by 63-81% (Egan et al. NEJM 2018;378:1691-1703). One interpretation of these findings is that treatment at the AD dementia stage is too late in the disease process. A second large trial (APECS; clinicaltrials.gov NCT01953601) was initiated in 2013 to evaluate verubecestat in participants with prodromal AD. Eligible participants had subjective memory decline with objective memory impairment and were amyloid positive (determined by amyloid imaging PET scan or CSF tau: Aβ42 ratio) but did not meet criteria for dementia. A decision to terminate the APECS trial was made in February 2018 following a recommendation by the external Data Monitoring Committee, which concluded that it was unlikely that positive benefit/risk could be established if the trial continued to its scheduled completion in 2019. Objectives: The objectives of this symposium are to present key efficacy and safety findings from the APECS trial and to have a panel of experts discuss the findings and implications for future development of BACE1 inhibitors. Results will be unveiled at CTAD. Discussion: The findings from the APECS trial suggest that blocking Aβ production at the prodromal AD stage does not slow clinical progression. Because the deposition of Aβ takes place years before the prodromal stage, it is possible that administration of an antiamyloid agent like verubecestat may be effective if given even earlier in the disease process. An alternative possibility is that the production of Aβ peptides may not play a major causal role in the pathophysiology of AD. Conclusions: Verubecestat was not effective in slowing clinical progression in participants with prodromal AD.","PeriodicalId":48606,"journal":{"name":"Jpad-Journal of Prevention of Alzheimers Disease","volume":"5 1","pages":"1-45"},"PeriodicalIF":6.4,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14283/jpad.2018.39","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66893385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying Better Outcome Measures to Improve Treatment of Agitation in Dementia: A Report from the EU/US/CTAD Task Force","authors":"Mary Sano, M. Soto, M. Carrillo, J. Cummings, S. Hendrix, J. Mintzer, A. Porsteinsson, P. Rosenberg, L. Schneider, J. Touchon, P. Aisen, B. Vellas, C. Lyketsos, Euusctad Task Force members","doi":"10.14283/jpad.2018.15","DOIUrl":"https://doi.org/10.14283/jpad.2018.15","url":null,"abstract":"For the second time in the past 3 years, the EU-US CTAD Task Force addressed challenges related to designing clinical trials for agitation in dementia, which is one of the most disruptive aspects of the condition for both patients and caregivers. Six recommendations emerged from the Task Force meeting: 1 – Operationalizing agitation criteria established by the IPA; 2 – Combining clinician- and caregiver-derived outcomes as primary outcome measures; 3 – Using global ratings to define clinically meaningful effects and power studies; 4 – Improving the accuracy of caregiver reports by better training and education of caregivers; 5 – Employing emerging technologies to collect near real-time behavioral data; and 6 – Utilizing innovative trial designs and increasing the use of biomarkers to maximize the productivity of clinical trials for neuropsychiatric symptoms.","PeriodicalId":48606,"journal":{"name":"Jpad-Journal of Prevention of Alzheimers Disease","volume":"5 1","pages":"98-102"},"PeriodicalIF":6.4,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.14283/jpad.2018.15","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66893315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}