NCT02854033: ADNI3

Alzheimer's Disease Neuroimaging Initiative 3

Completed Last updated 11 March 2026

What this trial tests

trial in Mild Cognitive Impairment (MCI) in 1,141 participants. Completed in 28 May 2024.

Timeline

2 December 2016

Primary endpoint
28 May 2024

28 May 2024

Quick facts

Lead sponsor	University of Southern California
Status	Completed
Study type	OBSERVATIONAL
Enrollment	1,141
Start date	2 December 2016
Primary completion	28 May 2024
Estimated completion	28 May 2024
Sites	59 locations across Canada, United States

Conditions studied

• Mild Cognitive Impairment (MCI) — all drugs for Mild Cognitive Impairment (MCI) →
• Alzheimer's Disease (AD) — all drugs for Alzheimer's Disease (AD) →

Sponsor

University of Southern California

Who can join

Adults 55 to 90, any sex, with Mild Cognitive Impairment (MCI) or Alzheimer's Disease (AD). Patients with the condition only — healthy volunteers not accepted.

Sponsor's own description

Since its launch in 2004, the overarching aim of the Alzheimer's Disease Neuroimaging Initiative (ADNI) has been realized in informing the design of therapeutic trials in AD. ADNI3 continues the previously funded ADNI-1, ADNI-GO, and ADNI-2 studies that have been combined public/private collaborations between academia and industry to determine the relationships between the clinical, cognitive, imaging, genetic and biochemical biomarker characteristics of the entire spectrum of Alzheimer's disease (AD). The overall goal of the study is to continue to discover, optimize, standardize, and validate clinical trial measures and biomarkers used in AD research.

Publications & conference data

8 peer-reviewed publications reference this trial (live from Europe PMC):

1. Functional brain architecture is associated with the rate of tau accumulation in Alzheimer's disease.
   Franzmeier N, Neitzel J, Rubinski A, Smith R, et al · · 2020 · cited 288× · PMID 31953405 · DOI 10.1038/s41467-019-14159-1
2. Functional connectivity associated with tau levels in ageing, Alzheimer's, and small vessel disease.
   Franzmeier N, Rubinski A, Neitzel J, Kim Y, et al · · 2019 · cited 189× · PMID 30770704 · DOI 10.1093/brain/awz026
3. Amyloid-associated increases in soluble tau relate to tau aggregation rates and cognitive decline in early Alzheimer's disease.
   Pichet Binette A, Franzmeier N, Spotorno N, Ewers M, et al · · 2022 · cited 96× · PMID 36333294 · DOI 10.1038/s41467-022-34129-4
4. The BIN1 rs744373 SNP is associated with increased tau-PET levels and impaired memory.
   Franzmeier N, Rubinski A, Neitzel J, Ewers M, et al · · 2019 · cited 85× · PMID 30992433 · DOI 10.1038/s41467-019-09564-5
5. Earlier Alzheimer's disease onset is associated with tau pathology in brain hub regions and facilitated tau spreading.
   Frontzkowski L, Ewers M, Brendel M, Biel D, et al · · 2022 · cited 73× · PMID 35987901 · DOI 10.1038/s41467-022-32592-7
6. Associations of longitudinal plasma p-tau181 and NfL with tau-PET, Aβ-PET and cognition.
   Rauchmann BS, Schneider-Axmann T, Perneczky R, Alzheimer's Disease Neuroimaging Initiative (ADNI). · · 2021 · cited 58× · PMID 34187867 · DOI 10.1136/jnnp-2020-325537
7. Early detection of amyloid load using ¹⁸F-florbetaben PET.
   Bullich S, Roé-Vellvé N, Marquié M, Landau SM, et al · · 2021 · cited 49× · PMID 33773598 · DOI 10.1186/s13195-021-00807-6
8. KL-VS heterozygosity is associated with lower amyloid-dependent tau accumulation and memory impairment in Alzheimer's disease.
   Neitzel J, Franzmeier N, Rubinski A, Dichgans M, et al · · 2021 · cited 47× · PMID 34158479 · DOI 10.1038/s41467-021-23755-z