Searching for simple principles beneath the complexity.
I’m a biophysicist and doctoral researcher in Uri Alon’s lab at the Weizmann Institute of Science. I use physics-inspired theory and quantitative analysis to uncover structure in the growing ocean of aging data.
I’m a biophysicist and systems biologist studying aging across scales and species. I combine physics-inspired models with demographic and mortality statistics, twin and longitudinal studies, comparative species data, and single-cell data to search for quantitative principles.
Before moving into biophysics, I completed my MSc in physics with a thesis in theoretical astrophysics.
In my free time, I enjoy reading long novels and watching old movies.
Lifespan heritability was long thought to be around 20–25%. We showed that accounting for extrinsic mortality raises the estimate for intrinsic lifespan to about 50%. However, the other half of the pie remains undetermined. Using data from the Swedish SATSA study, we are working on carving up the remainder: how much reflects lifestyle and environmental exposures, how much is developmental stochasticity fixed early in life, and how much is dynamic stochasticity accumulated over the life course?
How much of the variation in human lifespan is inherited? Combining twin data with mathematical modeling, we estimate that intrinsic lifespan is about 50% heritable after accounting for extrinsic mortality.
When does aging begin, and how do conditions at birth shape what follows? I study how development and neonatal vulnerability influence mortality across the lifespan, and whether the same stochastic framework can explain both the decline in mortality after birth and its rise in old age.
Mortality falls after birth and rises again in old age. We show how differences in neonatal vulnerability can produce the early decline within stochastic threshold models, linking both phases in a shared framework.
How much of aging can a one-dimensional stochastic equation capture? I use models in which damage accumulates, fluctuates, and eventually crosses a failure threshold to connect individual dynamics with patterns of morbidity and mortality across populations. These models let us ask which changes extend healthy life and which shift lifespan limits.
a Individual damage
b Death rate (log scale)
Each line is one simulated life: damage fluctuates and rises until it crosses a threshold (a). Together, these lives produce a death rate that climbs exponentially with age (b).
Why can typical lifespan improve while the longest lifespans change so little? Using a model of damage accumulation, we investigate how changes that improve survival can differ from those that extend maximal lifespan.
How much of the variation in human lifespan is inherited? Combining twin data with mathematical modeling, we estimate that intrinsic lifespan is about 50% heritable after accounting for extrinsic mortality.
Why do species age at such different rates, and why do some retain function longer than others? I compare mortality and functional trajectories across the tree of life to explore how ecology, life history, and evolutionary relatedness shape aging.
Budding yeast mother cells grow as they divide, then eventually stop reproducing. I study whether their size dynamics can help explain this replicative lifespan: how growth rates, fluctuations, and differences between cells relate to the timing of senescence. By combining single-cell measurements with stochastic models, I test the idea that approaching a size threshold contributes to this loss of reproductive capacity.
What would longer lives mean for the populations we live in? I connect models of aging interventions with demographic projections to explore changes in population size and age structure. I’m particularly interested in how these outcomes depend on when treatment begins, how widely it becomes available, and whether it slows aging or improves robustness.
How much of the variation in human lifespan is inherited? Combining twin data with mathematical modeling, we estimate that intrinsic lifespan is about 50% heritable after accounting for extrinsic mortality.
DOI 10.64898/2026.05.05.722841
Mortality falls after birth and rises again in old age. We show how differences in neonatal vulnerability can produce the early decline within stochastic threshold models, linking both phases in a shared framework.
DOI 10.64898/2025.12.22.695887
Why can typical lifespan improve while the longest lifespans change so little? Using a model of damage accumulation, we investigate how changes that improve survival can differ from those that extend maximal lifespan.
After neutron stars merge, radioactive decay heats the expanding material that powers a kilonova. We derive a simple analytic description of how beta-decay electrons deposit their energy, connecting this microscopic process to the evolving light.
Weizmann Institute of Science · Uri Alon’s lab
Weizmann Institute of Science
Thesis on neutron-star merger physics.
Hebrew University of Jerusalem
Amirim Interdisciplinary Honors Program in the Humanities
Take a look at some ongoing projects.
Questions, ideas, collaborations