Q&A
Yentli often describes her work as being shaped by a triple perspective: genetic carrier, scientist, and physician-in-training.
That combination changes the questions she asks. As a scientist, she sees the mechanistic gaps in the field. As a future physician, she sees how current systems fail families affected by genetic ALS and FTD. As a genetic carrier, she feels the urgency of delay in a deeply personal way.
Rather than focusing only on how to treat disease after symptoms appear, she is equally focused on how to detect disease earlier, how to predict whether a carrier may develop ALS or FTD, and how to build prevention strategies before irreversible damage takes hold.
That shift became personal after her father died from rapidly progressive ALS caused by the C9orf72 mutation — the same mutation she carries.
His death changed the direction of her work. Instead of staying within her original field, she turned toward one of the hardest and most urgent problems in neurodegeneration: how to prevent and cure the most common genetic cause of ALS and frontotemporal dementia.
Her transition was not just an academic pivot. It was a decision driven by survival, grief, and the belief that existing structures were not moving fast enough for families like hers.
At first, Yentli was trying to solve fragmentation.
The data, biological samples, prevention frameworks, and expertise needed to answer the biggest questions in C9orf72 disease are spread across institutions, countries, and disciplines. Rather than waiting for someone else to bring those pieces together, she began building the collaborations herself.
Over time, that effort became broader than one project. It grew into a networked strategy across research, infrastructure, community education, and advocacy — all aimed at changing the future for genetic carriers and their families.
CureC9 is a program within EverythingALS focused on the most common genetic cause of ALS and FTD: the C9orf72 repeat expansion.
Its mission is to bring strategic direction and focused support to the questions mainstream funding structures often overlook. Through an independent Scientific Advisory Board and a growing research network, CureC9 is designed to help identify the most important gaps in the field and direct energy, collaboration, and resources toward work that can change outcomes.
The goal is not only to fund research, but to help build a clearer path from scientific insight to prevention and, ultimately, cure.
Prevention is central because disease onset is often defined clinically, not biologically.
By the time someone is diagnosed with ALS or FTD, the disease process has already been unfolding for years. For genetic carriers, that means the window to intervene may begin long before symptoms appear — but only if researchers can detect and measure what is changing early enough.
Yentli believes that genetic carriers need more than a wait-and-see model. They need tools, biomarkers, and research frameworks that make prevention possible. That is why so much of her work focuses on presymptomatic monitoring, digital biomarkers, and building systems that could support future prevention trials.
Search for a Self Cure is a science communication and education initiative that helps translate complex ALS and FTD research into language genetic carriers and families can understand.
Through interviews, summaries, and accessible explanations, the project aims to reduce the distance between the people participating in research and the science shaping their future. It is rooted in the belief that patients and carriers deserve more than participation alone — they deserve meaningful access to the ideas, strategies, and discoveries their lives depend on.
For Yentli, it is also personal. It is a resource she wanted during one of the darkest periods of her life, and one she hopes can help others feel less lost.
Yentli’s approach is highly collaborative, strategic, and deeply personal.
Rather than building a traditional academic silo, she has focused on identifying gaps no single lab can solve alone, then bringing together the people needed to move those problems forward. That has meant building collaborations across countries, disciplines, and institutions — often from scratch.
Her role is not to claim every part of the work for herself, but to connect people, align effort, and help create the structure needed for meaningful progress.
Her father’s life and death are at the center of why this work exists.
He died from rapidly progressive C9orf72 ALS, and his illness transformed abstract scientific questions into immediate ones. His loss did not simply inspire the work emotionally; it helped define its urgency, direction, and structure.
Much of what Yentli is building is shaped by the desire to create a different future for other families — one in which genetic risk does not come with the same absence of options, roadmap, or hope.
The bigger goal is to build what does not yet exist: a more strategic, prevention-oriented, collaborative path toward survival for people at risk of C9orf72 disease.
That means better science, but also better infrastructure, better communication, and better frameworks for prevention. It means connecting researchers, carriers, and institutions around the work that matters most.
At its core, this is an effort to turn urgency into structure and structure into progress.