The CCNA COMPASS-ND study aims to investigate the bases, commonalities, and distinguishing characteristics of Alzheimer disease and related neurodegenerative disorders.
This study will test the safety and tolerability of a medium chain triglyceride (MCT) supplement in those with Alzheimer Disease (AD).
The purpose of this project is to conduct a proof of concept study in patients with probable Alzheimer's Disease who have mild to moderate hypertension, in order to determine if there is less global brain atrophy over one year, as measured by ventricular enlargement as a primary outcome measure, when patients are randomized to treatment with an angiotensin receptor blocker compared to an Angiotensin Converting Enzyme inhibitor (ACEI).
The purpose of this study is to assess the safety, tolerability, biomarker and cognitive efficacy of investigational products in subjects who are known to have, or are at risk of having an Alzheimer's disease-causing mutation by determining if treatment with the study drug slows the rate of progression of cognitive impairment and improves disease-related biomarkers.
This study also offers an observational component collecting cognitive assessment data until the availability of an enrolling drug treatment group, referred to as cognitive run-in (CRI).
The primary objective of the study is to evaluate the efficacy of monthly doses of aducanumab in slowing cognitive and functional impairment as measured by changes in the Clinical Dementia Rating-Sum of Boxes (CDR-SB) score as compared with placebo in participants with early AD.
The purpose of this study is to provide subjects who have completed participation in a Phase 2 or Phase 3 trial with TRx0237 continued access to therapy and to evaluate the long-term safety of TRx0237.
AZD0530 is an inhibitor of Src and Abl family kinases1. It has been developed as treatment for malignancies because these kinases play a role in tumor invasion and proliferation. However, the Src family kinases (SFKs) are highly expressed in brain and have major effects on synaptic plasticity2. Moreover, the investigators have recently shown that a specific SFK, namely Fyn, is aberrantly activated by specific conformations of the Amyloid Beta (Aß) peptide from Alzheimer's disease (AD). Genetic deletion of Fyn rescues AD deficits in preclinical models.
The purpose of this study is to determine the clinical, cognitive, motor, brain imaging, genetic and biochemical biomarker characteristics of Alzheimer disease (AD), subcortical vascular disease (SVaD) and mixed dementia (AD + sVaD).