Our research
Our research focuses on understanding why individuals age differently, with particular emphasis on cardiometabolic health and cognitive aging. One line of work examines heterogeneity in obesity, distinguishing genetically versus environmentally driven adiposity, the role of metabolic health, and age-specific changes. A parallel line studies life course risk factors for dementia and leverages recent advances in blood-based biomarkers to characterize preclinical trajectories and study causal risk factors and resilience.
The heterogeneity of obesity and cardiometabolic aging
Cardiometabolic risk factors such as obesity, dyslipidemia, and hypertension are strongly linked to morbidity and mortality in later life, yet their consequences vary widely between individuals. Our research examines obesity and cardiometabolic health as heterogeneous and dynamic processes rather than static risk states. We study how genetic predisposition, lifestyle, metabolic profiles, sex, and life stage influence associations between obesity and risk of e.g. cardiovascular disease, type 2 diabetes, dementia, and survival. By integrating longitudinal cohort data with genetically informed designs, we aim to disentangle causal effects from reverse causation and confounding, refine risk assessment beyond BMI, and inform more individualized and less stigmatizing approaches to cardiometabolic prevention in aging populations.
Life‑course pathways to dementia and brain aging
Dementia develops over decades, with a long preclinical phase during which pathological brain changes accumulate silently. Our research investigates how life-course exposures, cardiometabolic factors, and genetic susceptibility shape trajectories toward cognitive decline and dementia, as well as why some individuals remain cognitively resilient despite substantial pathology. We combine longitudinal twin studies, population-based cohorts, and blood-based biomarkers of neurodegeneration and Alzheimer’s disease, together with multi-omics data, to study early disease mechanisms and strengthen causal inference. A major focus is the use of new blood‑based biomarkers to identify biological pathways linking modifiable risk factors to neurodegenerative and vascular processes, and to develop interpretable prediction models that improve early identification and stratification of dementia risk in the general population.
This theme also includes work within the Interplay of Genes and Environment across Multiple Studies (IGEMS) consortium, a collaboration involving over fifteen longitudinal twin studies of adult development and aging. Ongoing projects in IGEMS include work to strengthen or refute causal hypotheses and test gene-environment interplay among modifiable factors for dementia risk and resilience, and how country, cohort, and gender disparities influence the relationship between education and dementia.
SATSA – The Swedish Adoption/Twin Study of Aging
Our work includes The Swedish Adoption/Twin Study of Aging(SATSA); PI Ida Karlsson & Sara Hägg), a unique cohort of twin pairs with almost 30 years of follow-up. The rich data includes a broad spectrum of biological, psychological, and social domains, collected in up to 9 waves of questionnaires and 10 waves of in-person testing. The longitudinal follow-up provides opportunities for detailed examinations of individual differences in age-related health, and the twin design provides possibilities to examine the importance of genetic and environmental influences and a quasi-causal setting to compare disease-discordant twin pairs.