scholarly journals What We Learn from the CTAD 2018 (Clinical Trials Alzheimer’s Disease)

2018 ◽  
pp. 1-2
Author(s):  
B. Vellas ◽  
P. Aisen ◽  
M. Weiner ◽  
J. Touchon
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Trials ◽  
Safety Data ◽  
Phase Iii ◽  
Drug Trials ◽  
New Developments ◽  
Fda Guidance ◽  
Clinical Biomarkers ◽  
Early Alzheimer’S Disease

We are happy to publish the CTAD 2018 abstracts in the present JPAD issue. As you can see many new interesting studies are presented in this issue of the journal: from new drug trials to biomarkers, imaging studies, as well as new clinical outcomes. More specifically, we will have several hot topics presentation on: 1. Major drug trials using bace inhibitors (verubecestat, lanabecestat, atabecestat, elenbecestat…) in the early phase of the disease (APECS early trials…). Both clinical, biomarkers (MRI, CSF, PET) and safety data will be presented. 2. New data on blood biomarkers including a keynote from R. Bateman, and presentations from Araclon and Roche biomarkers. 3. Results from phase III and IIB trials including a novel and multi-targeted oligosaccharide in patients with mild-moderate AD in China; the AMBAR (Alzheimer’s Management By Albumin Replacement) study, the TOMMORROW trial: a trial to delay the onset of MCI due to AD and qualify a genetic biomarker algorithm, the 18-month STEADFAST trial of azeliragon in participants with mild Alzheimer’s Disease; a longitudinal 148-week extension 4. Results 18 from F-AV-1451-A16: a clinicopathological study of the correspondence between flortaucipir PET imaging and post-mortem assessment of tau pathology. 5. Latest developments in anti-amyloid monoclonal antibodies including aducanumab nonnegligible, and new results and data analyses of the BAN2401 study 201 in early AD. 6. New developments with safety and efficacy of lemborexant for sleep-wake regulation in patients with irregular sleep-wake rhythm disorders and Alzheimer’s Disease dementia. 7. Advances with the ABBV-8E12, a humanized anti-tau monoclonal antibody, for the treatment of early Alzheimer’s Disease. 8. Endpoints for early Alzheimer’s Disease clinical trials: interpretation and application of the draft FDA guidance. And many others… It is important to underline that a not negligible number of abstracts concern non amyloid targets (eg: Tau-related targets but also targets outside the classical AD cascade).

CONFUSION IN CLINICAL TRIALS OF ALZHEIMER'S DISEASE

2015 ◽  
Vol 86 (11) ◽  
pp. e4.137-e4
Author(s):  
Jeremy Hobart ◽  
Sophie Cleanthous ◽  
John Zajieck ◽  
Stefan Cano
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Trials ◽  
Clinical Outcome ◽  
Treatment Effectiveness ◽  
Measurement Properties ◽  
Assessment Instruments ◽  
Evidence Based ◽  
Fda Guidance ◽  
Literature Reviews

BackgroundNeurology clinical trials frequently use clinical outcome assessment instruments (COAs) as outcome measures. We question the extent to which measurement limitations of COAs contribute to clinical trials failures in Alzheimer's disease.ObjectivesWe conducted a series of literature reviews to: identify the concepts assessed in AD clinical trials, and how these concepts were defined and measured; identify which COAs have been used in AD clinical trials, and on which grounds they were selected. We examined published measurement properties of COAs used in AD clinical trials in accordance with FDA guidance.ResultsA set of literature reviews identified >6500 publications from PUBMED/EMBASE inception. In the extracted 850 articles, 984 uniquely named concepts were assessed and 1283 COAs were used. However, few trials provided definitions of the concepts they measured; very different COAs were used to measure the same (named) concepts; the same COAs were used to measure different concepts; COA selection was rarely justified or evidence-based. Further reviews of COA development papers (n=174) indicated most fail to meet recommended criteria.ConclusionsFindings imply substantial measurement confusion in AD clinical trials and suggest they have provided weak evaluations of treatment effectiveness. Findings were replicated in Parkinson's disease (n366 articles).

Learning from the Past: A Review of Clinical Trials Targeting Amyloid, Tau and Neuroinflammation in Alzheimer’s Disease

2020 ◽  
Vol 17 (2) ◽  
pp. 112-125 ◽  
Author(s):  
Kelly Ceyzériat ◽  
Thomas Zilli ◽  
Philippe Millet ◽  
Giovanni B. Frisoni ◽  
Valentina Garibotto ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Trials ◽  
Animal Models ◽  
Phase Iii ◽  
Current Status ◽  
Central Feature ◽  
Phase Iii Trial ◽  
The Past ◽  
Positive Results

Alzheimer’s Disease (AD) is the most common neurodegenerative disease and cause of dementia. Characterized by amyloid plaques and neurofibrillary tangles of hyperphosphorylated Tau, AD pathology has been intensively studied during the last century. After a long series of failed trials of drugs targeting amyloid or Tau deposits, currently, hope lies in the positive results of one Phase III trial, highly debated, and on other ongoing trials. In parallel, some approaches target neuroinflammation, another central feature of AD. Therapeutic strategies are initially evaluated on animal models, in which the various drugs have shown effects on the target (decreasing amyloid, Tau and neuroinflammation) and sometimes on cognitive impairment. However, it is important to keep in mind that rodent models have a less complex brain than humans and that the pathology is generally not fully represented. Although they are indispensable tools in the drug discovery process, results obtained from animal models must be viewed with caution. In this review, we focus on the current status of disease-modifying therapies targeting amyloid, Tau and neuroinflammation with particular attention on the discrepancy between positive preclinical results on animal models and failures in clinical trials.

Designing drug trials for Alzheimer's disease: What we have learned from the release of the phase III antibody trials: A report from the EU/US/CTAD Task Force

2013 ◽  
Vol 9 (4) ◽  
pp. 438-444 ◽  
Author(s):  
Bruno Vellas ◽  
Maria C. Carrillo ◽  
Cristina Sampaio ◽  
H. Robert Brashear ◽  
Eric Siemers ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Task Force ◽  
Phase Iii ◽  
Drug Trials ◽  
The Eu

Novel approaches to incorporating pharmacoeconomic studies into phase III clinical trials for Alzheimer's disease

2010 ◽  
Vol 14 (8) ◽  
pp. 640-647 ◽  
Author(s):  
H. Fillit ◽  
J. Cummings ◽  
P. Neumann ◽  
T. Mclaughlin ◽  
P. Salavtore ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Trials ◽  
Phase Iii ◽  
Phase Iii Clinical Trials ◽  
Novel Approaches

P4-178: RATER QUALIFICATIONS IN EARLY ALZHEIMER'S DISEASE CLINICAL TRIALS

2014 ◽  
Vol 10 ◽  
pp. P854-P854
Author(s):  
Macarena García-Valdecasas Colell ◽  
Julie Marsh ◽  
Jan Sedway
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Trials ◽  
Early Alzheimer’S Disease

scholarly journals New Approacher in the Development of Alzheimer’s Disease Modifying Drugs

2021 ◽  
pp. 88
Author(s):  
◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Trials ◽  
Tau Protein ◽  
Phase Iii ◽  
Disease Modifying Drugs ◽  
Phase Iii Clinical Trials ◽  
Research Level ◽  
Disease Modifying ◽  
Pathological Stages

Introduction: Alzheimer’s disease is a more common neurodegenerative disease, affecting 25 million people worldwide, or accounting for about 60 to 70% of all dementia cases. There is currently no exact mechanism to explain the pathophysiology of Alzheimer’s disease, however, cascading metabolic amyloid and post-translational review of tau protein are used as major hypotheses. Objective: To demonstrate in the literature new approaches in the development of Alzheimer’s disease modifiers. Methodology: For the accomplishment of this study made in the bibliographical survey of scientific literature and respect to the approached subject, in the databases PUBMED, ScienceDirect, Scielo and Scopus. Results: Alzheimer’s disease-modifying drugs are not yet available, but many patients may, however, develop phase III clinical trials and are intended to modify as pathological stages leading to the disease. As disease-modifying therapies under study, these changes also affect Aβ and tau protein and also cause inflammation and oxidative damage. The results obtained in the clinical trials performed were positive and promising and are still under study. The results show that there is still a long way to go in the development of Alzheimer’s disease modifying drugs. Conclusion: The results demonstrated that there is still a long way to go in the development of Alzheimer’s disease modifying drugs, but nevertheless levels at the research level should be continued in order to improve the pathophysiology of the disease and find an effective treatment for this disease the same.

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