There are many active research projects accessing and applying shared ADNI data. Use the search above to find specific research focuses on the active ADNI investigations. This information is requested annually as a requirement for data access.
| Principal Investigator | |
| Principal Investigator's Name: | Courtney Vehling |
| Institution: | Eli Lilly & Company |
| Department: | Global Patient Outcomes & Real World Evidence |
| Country: | |
| Proposed Analysis: | Identify and describe a TB2-like historical control cohort with baseline imaging biomarkers (amyloid and tau) and longitudinal outcomes (especially iADRS) data. Enables comparison of long-term (3 year) outcomes from TRAILBLAZER-ALZ2 open-label extension (AACJ) to modeled historical control, addressing key payer concerns regarding long-term donanemab treatment efficacy |
| Additional Investigators | |
| Investigator's Name: | Joseph Johnston |
| Proposed Analysis: | Identify and describe a TB2-like historical control cohort with baseline imaging biomarkers (amyloid and tau) and longitudinal outcomes (especially iADRS) data. Enables comparison of long-term (3 year) outcomes from TRAILBLAZER-ALZ2 open-label extension (AACJ) to modeled historical control, addressing key payer concerns regarding long-term donanemab treatment efficacy |
| Investigator's Name: | Julie Chandler |
| Proposed Analysis: | Identify and describe a TB2-like historical control cohort with baseline imaging biomarkers (amyloid and tau) and longitudinal outcomes (especially iADRS) data. Enables comparison of long-term (3 year) outcomes from TRAILBLAZER-ALZ2 open-label extension (AACJ) to modeled historical control, addressing key payer concerns regarding long-term donanemab treatment efficacy |
| Investigator's Name: | Wendy Ye |
| Proposed Analysis: | The aim of these analyses was to examine long term cognitive, functional and behavioral outcomes in persons with biomarker confirmed early Alzheimer’s Disease (MCI and Mild AD). We specifically examined 1) the impact of different rates of disease progression (defined as change in cognitive function as measured by CDR-SB over the first year) on important outcomes such as cognition, function and behavior) over the subsequent 4-5 years and 2) the implications of slowing disease progression by 20-30% on those outcomes. Two cohorts from different sources were identified to explore these questions: National Alzheimer’s Coordinating Center (NACC) Uniform Data Set in the US and the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database. In both cohorts, individuals with a clinical assessment of Mild Cognitive Impairment or mild dementia, a CDR-SB score of 0.5-9 at the first visit, and confirmed amyloid positivity were included. For the first analyses examining rates of disease progression , participants were stratified into no or slow progression, median progression and fast progression based on change in CDR-SB at the first year. There were 1263 eligible NACC participants and 495 eligible ADNI participants. For each cohort (analyzed separately), the cognitive (CDR-SB), functional (FAQ) and neuropsychiatric (NPI-Q) outcomes were described for the initial visit and each subsequent visit up to 5 years. Our results showed that participants classified as ‘faster’ progressors based on first year change in CDR-SB had worse scores on CDR-SB, FAQ, and NPI-Q at the first visit, despite similar age, gender and comorbidity profiles. Over 4-5 years of follow up the faster progressors demonstrated greater deterioration in all cognitive, functional and behavioral performance than the slow or median progressors. Results from the ADNI cohort were generally consistent with those from the NACC cohort. This retrospective, real-world study finds that despite similar demographic and comorbidity profiles at baseline, individuals with confirmed brain amyloid pathology with faster cognitive progression early in the disease trajectory experienced higher impairment of cognitive and functional outcomes over time compared to those with more gradual change in early disease stages. These findings underscore the importance of early intervention among individuals with AD. With the recent availability of potentially disease-modifying therapies for individuals with biomarker-confirmed early AD, the current study findings provide important insights to optimize the long-term care of this complex disease. The second analysis focused on implications of slowing disease progression on functional and behavioral outcomes. Hypothetical effects of slowing CDR-SB decline by 20 to 30% on functional and behavioral outcomes over 4-5 years were evaluated using multivariable regression. The NACC and ADNI cohorts were analyzed separately. For the NACC cohort, in response to slowing disease progression by 20% over five years relative to natural progression (i.e., 0% slowing), the model projects a lesser FAQ score increase by 10.8% for MCI participants and 12.9% for those with dementia. A 20% reduction in disease progression was associated with a slower decline in NPI-Q by 0.5 points (20.3% difference) for the MCI cohort and 0.5 points (19.3% difference) for those with early dementia, compared with natural progression. For the ADNI analysis, only the MCI participants were used for the analysis due to sample size limitations in the Mild dementia group. The model projects that delaying disease progression (i.e., reduced CDR-SB) by 20% or 30% at year 4 would preserve functional ability (as measured by FAQ) by 19.7% and 29.6%, respectively, compared to natural disease progression. Taken together, these findings help quantify the potential value of slowing disease progression with emerging treatments among participants with confirmed amyloid pathology in the early stages of symptomatic AD from patient, caregiver, and health system perspectives. |
