Background
Alzheimer’s disease (AD) is the leading cause of dementia worldwide. The pathological brain changes begin to develop long before clinical symptoms emerge. Understanding these earliest biological processes is essential for the development of diagnostic tools and preventive strategies.
Objective
The ASIC-E4 project examined some of the earliest biological signals of AD in cognitively normal older adults. Conducted at the Turku PET Centre in collaboration with the University of Gothenburg, the study focused on a cohort uniquely selected based on APOE genotypes corresponding to differing levels of genetic risk for late onset AD. By combining PET imaging, MRI, extensive cognitive testing, and blood based biomarker analyses, the research team aimed to clarify how amyloid accumulation, neuroinflammation, and synaptic loss emerge and interact long before clinical symptoms appear.
The role of Auria Biobank in recall of study participants
Auria Biobank played a crucial enabling role in the ASIC‑E4 project by supporting targeted recruitment of a uniquely characterized study population. Through biobank consent and an additional permission for recontacting, the biobank was able to identify and invite potential participants based on existing data on APOE genotype. This collaboration made it feasible to recruit rare APOE e4/e4 homozygotes—an otherwise highly challenging task—and ensured that all participants were recruited in a compliant, ethically robust manner.
“Without smooth collaboration with Auria Biobank it would have been practically impossible to recruit a decent number of participants with the rare APOE genotype (e4/e4) timely and cost-effectively" says Professor Juha Rinne from Turku PET Centre, University of Turku and Turku University Hospital, Turku, Finland.
From study design to published results
The original ASIC‑E4 study protocol included a planned follow‑up approximately four years after baseline to support longitudinal analyses of cognitive performance and biomarker changes. To date, the project has generated high‑quality cross‑sectional results, reported in peer‑reviewed publications, demonstrating how genetic risk, amyloid burden, neurodegeneration, cerebrovascular pathology and blood biomarkers are interrelated already in cognitively unimpaired individuals. In particular, the most recent publication (Koivumäki et al., 2024) reports detailed single‑time‑point imaging and blood biomarker analyses, highlighting subtle but biologically meaningful differences between the APOE genotype groups and clarifying how different brain pathologies contribute to circulating biomarkers of neurodegeneration.
Why this matters
ASIC‑E4 illustrates how close collaboration between a research team and a hospital‑integrated biobank can enable studies that would otherwise be extremely difficult to implement. By combining genotype‑directed recruitment, advanced imaging infrastructure and deep phenotyping, the project provides a valuable foundation for future longitudinal research and for the development of early biomarkers in AD.
“Auria Biobank is proud to enable high‑impact research together with researchers with world‑class clinical and imaging expertise” says Auria Biobank’s Director Lila Kallio.
Fingenious® service, operated by Finnish Biobank Cooperative – FINBB, is a gateway to Finnish biobanks and biomedical research that offers researchers easy access to high-quality public biobank samples, data, cohorts, and recruitable study participants. FINBB aims to enhance the competitiveness of Finnish health and biomedical research by providing researchers with centralized access to collections and services of the Finnish biobanks and their background organizations. FINBB's activities create value for its members and owners by providing services at the national level. FINBB is a cooperative owned by five wellbeing services counties, HUS, six large universities in Finland, and the Finnish Institute for Health and Welfare (THL). FINBB has eight member biobanks.
Read more:
Snellman et al. 2022 https://doi.org/10.3389/fneur.2022.826423
Snellman et al. 2024 https://doi.org/10.1002/alz.14327
Koivumäki et al. 2024 https://doi.org/10.1186/s13195-024-01477-w
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