Clinical Trials

The purpose of this study is to measure target engagement in cerebrospinal fluid (CSF) and blood, and to establish the feasibility and safety of Dasatinib plus Quercetin treatment in adults with early stage but symptomatic Alzheimer's Disease (AD) to inform and select the best blood, CSF, urine, and other analyses to conduct in banked samples from a larger Phase 2b clinical trial.

The purpose of this study is to learn more about amyloid and tau burden in the brain of patients with Atypical Alzheimer's Disease and how that burden may change over a two-year period.

The purpose of this study is to optimize profile questionnaire and matching algorithm developed in Phase I and implement in final website design, and to determine if algorithmically matched participants have statistically significant increase in match satisfaction and self-reported sense of resiliency and quality of life over randomly matched caregivers.

The purpose of this study is to characterize and study the relationship of the clinical risk factors and predictors of seizures and epilepsy in patients with Early Onset Alzheimer's Disease (EOAD) using a 48-hour CAA-EEG.

The START study is a multicenter randomized, double-blind, placebo-controlled Phase 2 study designed to evaluate the efficacy, safety, and tolerability of two doses of CT1812 compared to placebo for approximately 18 months (72 weeks) in approximately 540 participants diagnosed with early Alzheimer’s disease.

This study is a public-private partnership with shared leadership responsibility across the Alzheimer’s Clinical Trial Consortium (ACTC) and Cognition Therapeutics, Inc.

Participants will be enrolled across approximately 50-60 clinical sites in the United States.

This is a multicenter randomized, double-blind, placebo-controlled Phase 2 study designed to evaluate the efficacy, safety, and tolerability of two doses of CT1812 compared to placebo in participants diagnosed with early Alzheimer's disease.

The overall purpose of this research is to understand how ADAD develops in order to eventually provide treatments for this disorder. Each biological child of a person with an ADAD mutation has a 50% risk of inheriting the mutation, and thus of developing ADAD. This study will develop a registry of families with a known ADAD mutation and will collect, analyze and bank data, tissue, and brain images from the members who participate in the DIAN research study. The data and tissue collected are available to all qualified researchers who wish to determine what changes occur before and after ADAD symptoms start. This understanding may lead to better tests and treatments for ADAD.

This study aims to establish, use, and extensively share a comprehensive longitudinal resource of genetic, non-genetic, and cognitive data, brain imaging and fluid biomarker measurements of amyloid-β (Aβ), tau pathophysiology, neurodegeneration, and inflammation (“A,T,N,I”), and biological samples to advance the study of cognitively unimpaired older adults at six levels of genetic risk for Alzheimer’s disease (AD) due to their apolipoprotein E (APOE) genotype, including understudied APOE2 and APOE4 homozygotes (HMs) at the lowest and highest risk and those APOE4 HMs and heterozygotes (HTs) who remain unimpaired at older ages due to unknown protective factors and spared pathophysiological effects despite their genetic risk.

The purpose of this Longitudinal Early-onset Alzheimer's Disease Study (LEADS) is designed to look at disease progression in individuals with early onset cognitive impairment . Clinical/cognitive, imaging, biomarker, and genetic characteristics will be assessed across three cohorts: (1) early onset Alzheimer's Disease (EOAD) participants, (2) early onset non-Alzheimer's Disease (EO-nonAD) participants,and (3) cognitively normal (CN) control participants.

There is evidence that neurodegenerative changes precede clinical symptoms in Alzheimer’s disease by two decades (Villemagne et al, 2013). Early detection is critical for development of interventions to halt, slow, or even reverse these pathological processes. The promise of plasma biomarkers to identify early pathology is growing rapidly (Palmqvist et al, 2020), however it is likely that multiple converging biomarkers will be necessary to identify the earliest pathological changes, as subtle differences from healthy controls may fall within the margin of error for any given single biomarker measure. Here we propose that the evaluation of speech and language for both baseline (cross-sectional) and longitudinal changes (within-participant) may add significant value to early pre-clinical pathological changes in MCI and AD. This is bolstered by emerging evidence of the relationship between language characteristics and amyloid burden (Verfaillie et al, 2019) and the large literature that characterizes language-use differences and deficits across the spectrum of cognitive decline (e.g., Mueller et al, 2018). We propose to add a series of in-clinic language elicitation tasks that allow for automated assessment of relevant speech and language domains and to validate these measures cross-sectionally and longitudinally relevant to neuropsychological, blood, and PET biomarkers.