Employee Spotlight: Laura Grasso, Principal Scientist
Please tell us about your scientific career so far and what attracted you to join Harness Therapeutics back in 2020?
I am a cell biologist by training. I obtained my PhD at the University of Dundee, where I worked on differentiating mouse embryonic stem cells (mESCs) into neuronal cells. I became fascinated by the morphology of these cells, sparking my interest in neuroscience and desire to understand where the cellular process goes wrong in neurodegeneration.
To pursue this interest, I moved to Cambridge for a postdoctoral position at the MRC Laboratory of Molecular Biology, where I worked with an in vivo model of Parkinson’s Disease (PD). My project focused on testing a small molecule and its potential effects in a PD mouse model.
After my postdoc, I was certain that I wanted to continue in the neuroscience field and contribute to efforts aimed at tackling neurodegeneration. I joined Harness Therapeutics almost five years ago, drawn by its novel and revolutionary approach of upregulating targets of interest, in contrast to the traditional strategy of downregulation. I was aware that this approach was highly challenging, but I also believed that, if successful, it could be truly groundbreaking and reshape current perspectives on neurodegeneration.
As a Principal Scientist, what does a typical day look like and what kind of projects are you currently working on?
Like everyone at Harness Therapeutics, my days are very busy and split between desk-based tasks and hands-on lab work. I am the project lead for our main program, which focuses on Huntington’s Disease (HD).
Part of my role involves coordinating with other team members, capturing ongoing activities, sharing updates with the project manager, and discussing potential next steps. I continuously assess our progress and look for any gaps or areas we might be overlooking. A typical day in the lab can range from simple tasks like ‘feeding’ neurons to more time-consuming experiments, such as running multiple assays to test ASO activity.
I’m also part of the development team, which is focused on bridging preclinical research into clinical studies, an incredibly interesting area and a great learning opportunity.
Why is working in the neurodegenerative space important to you?
As life expectancy increases, more and more people are likely to be affected by neurodegenerative diseases. My dedication to this field comes from a personal desire to help the people we love – not only our grandparents, but also ourselves, our partners, and even our children who might face these conditions in the future.
Neurodegenerative diseases and their associated cognitive decline are common in older populations and significantly impact both lifespan and quality of life. I often think about how difficult it must be to live with a condition that progressively reduces cognitive function, leading to a loss of independence and the need for constant support. It’s devastating not only for the patient but also for their family, who witness this slow decline. I want to be part of the effort to stop or slow down this process by contributing to research that can truly make a difference in people’s lives.
What's the most exciting breakthrough or discovery you've been part of during your time at Harness Therapeutics?
One of the biggest challenges in neurodegeneration research is selecting the right cellular model. The complexity arises from the fact that the most affected brain regions are often deep structures, making them difficult to model accurately. I was therefore excited to contribute to the development of a relevant cellular model for testing our antisense oligonucleotides (ASOs) in Huntington’s Disease (HD). Our goal is to slow down the CAG triplet repeat expansion in the huntingtin protein (HTT) gene, which has recently been shown to drive the molecular pathogenesis of HD. We are designing ASOs to target FAN1, a nuclease which could delay CAG expansion, and upregulate its protein expression.
To validate these ASOs, we needed a cellular model that was suitable for a functional readout of CAG expansion. I was involved in selecting and characterizing excitatory neurons, which, along with striatal cells, are among the most affected in HD. We now have two robust cellular models that are fundamental to assessing ASO efficacy and advancing a lead candidate.
Looking ahead, what emerging aspects of cell and molecular biology in the neurodegenerative space are you most excited about?
I believe one of the most significant recent achievements in the neurodegeneration field is the improved understanding of the molecular pathogenesis underlying different diseases. Although many neurodegenerative disorders have been known for decades, it has remained incredibly difficult to pinpoint exactly what causes them.
Recently, there's been a growing wave of interdisciplinary research aimed at characterising disease-associated proteins, understanding their functions, and exploring how they are regulated. One of the most exciting aspects is the use of omics approaches, particularly at the single-cell level. These provide detailed insights by contextualising what is happening, and where, within individual cells.
Additionally, advancements in more complex cellular models, such as 3D systems, are proving invaluable in better mimicking brain-like environments. These models bring us closer to replicating the real conditions of the human brain.
What excites me most is the convergence of different methodologies, from the development of advanced cell models to novel approaches for assessing drug activity. This cross-disciplinary integration is incredibly powerful and holds real promise for driving breakthroughs in the field.