The early mechanisms of brain aging remain poorly understood, because the pathological processes that lead to Alzheimer's disease begin decades before symptoms appear. At ages 50-69, cognitively healthy people already show subtle changes at the molecular, structural and physiological levels, but catching them one by one is nearly impossible. Large open databases such as ADNI or OASIS are disease-oriented and provide only coarse phenotyping, while deep studies tend to be small and scattered. COFITAGE stands apart: it is the first open cohort to combine PET, advanced MRI, polysomnography, APOE genotype and detailed neuropsychology in the same people within a key age window.
The study enrolled 101 French-speaking residents of Belgium (68 women) with no neurological or psychiatric disorders, normal sleep (apnea-hypopnea index < 15/h) and no use of psychoactive substances. A 3 Tesla MRI scanner produced high-resolution anatomical images, multiparametric maps (T1, proton density, magnetization transfer) and multishell diffusion (b = 650, 1000, 2000 s/mm²). PET with fluorine-18 florbetapir or fluorine-18 flutemetamol assessed amyloid burden in 100 people, and fluorine-18 THK5351 assessed tau pathology in 67. Two nights of polysomnography with 11 EEG leads captured sleep architecture, and genotyping on an Illumina chip determined APOE ε2/ε3/ε4 alleles. A neuropsychological battery of 15+ tests covered attention, executive function, memory, language and cognitive reserve. All data were converted to BIDS and checked with a validator.
The dataset includes 101 participants with a full set of modalities at baseline and 65 people who repeated cognitive testing after two years. Amyloid PET was performed in 100 people (97 with flutemetamol, 3 with florbetapir), tau PET in 67, and both modalities are available for 66. The MRI data include T1-weighted images with a 1×1×1 mm³ voxel, T2-weighted hippocampal slice images with a 0.4×0.4×1.2 mm³ voxel, multiparametric maps and diffusion with three shells. Polysomnography was recorded over two nights for each participant, with automatic scoring of sleep stages in 30-second epochs. APOE genotype was determined for everyone, and the allele distribution matches the population. Data quality was confirmed by the BIDS validator, and two participants with an orientation discrepancy in MTw scans are documented for users.
COFITAGE differs from neighboring open cohorts not in scale but in depth: a single sample brings together molecular, structural, physiological and cognitive layers that are usually studied separately. This makes it possible to test hypotheses about how amyloid, tau, sleep and cognitive reserve interact at the individual level, not just on average across a group. The work does not unveil a new biomarker, but it lays the foundation for such discoveries: these data have already shown that cortical reactivity and daytime fluctuations in brain activity are more sensitive to early aging than static measures. For researchers of brain aging, a resource like this is worth more than a large but shallow database.
The dataset will keep growing: upcoming releases will add raw polysomnography recordings, EEG, EEG-TMS, saliva and urine samples, actimetry, and a seven-year cognitive follow-up for roughly 65 participants. This will make it possible to move from cross-sectional associations to longitudinal trajectories and to test which baseline measures predict individual changes after seven years. The open BIDS structure invites the development of new methods for multimodal fusion and machine learning on deeply phenotyped but small samples.
The resource will directly affect research on preclinical Alzheimer's disease, hippocampal vulnerability, amyloid-tau interaction, sleep modulation of molecular pathology and cognitive reserve. It will also serve as a testing ground for methodological advances in image processing, multimodal data fusion and reproducible neuroimaging pipelines.
The immediate next step is the release of derived data (quantitative MRI maps, regional PET values) and extended phenotypic tables. In parallel, the seven-year follow-up is under way, and its results will be included in future releases.
For the neuroscience of aging, COFITAGE closes the gap between early molecular changes and cognitive decline: for the first time, a single sample allows researchers to test how amyloid, tau, sleep and reserve interact before symptoms appear. This addresses a key unresolved question: why do some people with pathology keep their cognition while others do not? The data also make it possible to separate normal aging from the prodromal stage of Alzheimer's disease, which is impossible in clinical cohorts.
COFITAGE participants slept in the laboratory two nights in a row to rule out the first-night effect, and their sleep during the week before recording was tracked with an actigraph and a diary. Such a rigorous protocol is rarely found in neuroimaging cohorts.
Not published on arXiv. Here are its page, the PDF and the formalization: you can check it yourself, not only read our account.