Our Research

Understanding a rare disease to understand us all.

Hutchinson–Gilford Progeria Syndrome compresses many hallmarks of aging into childhood. Here's how we're studying it — and what it might teach us about aging more broadly.

The Central Question

One gene. Two timelines.

Hutchinson–Gilford Progeria Syndrome arises from a single mutation in the LMNA gene, producing a toxic protein fragment known as progerin. In children who carry it, many of the biological hallmarks associated with old age appear within a matter of years.

Studying how one genetic change compresses a lifetime of cellular aging into childhood gives us a rare, sharpened lens on the much slower process every one of us goes through — and a chance to ask whether the two are more related than they first appear.

HGPSCompressed

Hallmarks of aging emerge in childhood — a fraction of a typical lifespan.

Typical AgingGradual

The same broad categories of cellular change, unfolding across decades.

Three ways in

How we're studying it

Illustration of a DNA strand highlighting a single point mutation
Genomics

Mapping how progerin reshapes the genome

We study how lamin A and its truncated form, progerin, alter chromatin organization — identifying which regions of the genome are affected, and how those changes ripple outward to affect gene expression more broadly.

This work combines sequencing approaches with computational analysis to build a genome-wide picture of what HGPS actually does at the molecular level, beyond its visible symptoms.

Researcher examining a sample under a microscope
Stem Cell Biology

Modeling the disease outside the body

We reprogram skin cells donated by HGPS patients into induced pluripotent stem cells (iPSCs), then guide them back into the tissue types the disease affects most — allowing us to watch the disease unfold in a dish, in real time.

This patient-derived model lets us test potential interventions in a way that would be impossible to do safely in a living patient.

Illustration of stem cells dividing inside a petri dish
Normal Aging

Testing the link to aging everyone experiences

A central question in the lab: are the mechanisms driving Progeria simply dialed-down, slower versions of what happens to all of us across a normal lifespan?

We test this by comparing molecular signatures between HGPS models and normally-aged tissue, looking for shared pathways that might one day be therapeutic targets for aging broadly, not just HGPS specifically.

Read our published findings

Our full list of publications and preprints is maintained separately — browse the complete archive there.

View Publications
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