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Student Q&A: Rummi Ganguly, NUIN

Rummi Ganguly

Rummi Ganguly, student in the Northwestern University Interdepartmental Neuroscience (NUIN) program, studies epilepsy-associated mutant sodium channel dysfunction in the laboratory of Alfred George, Jr., MD, chair and the Alfred Newton Richards Professor of Pharmacology.

Read a Q&A with Ganguly below.

Where is your hometown?

I grew up in Portland, OR. Keep it weird!

What sparked your interest in science or medicine?

My interest in science and medicine is rooted in my curiosity about the world and a desire to help people. I find it endlessly fascinating that every observation I have and will ever make is the complex product of measurable mechanisms of action at the smallest of scales. My natural tendency to question “why,” “what” and “how” is well-exercised in this field, and the idea of identifying and quantifying these mechanisms in pursuit of the diagnosis and treatment of human disease is most fulfilling.

What are your research interests?

I wish to connect molecular and cellular processes to systems level phenomenon and clinical phenotypes. I am specifically interested in utilizing computational methods in the diagnosis, analysis and treatment of neurological disease. In my current work, I use electrophysiological and computational techniques in the characterization of epilepsy-associated mutant sodium channel dysfunction to examine its influence on neuronal excitability and epilepsy phenotype.

What are you currently working on?

There exists a gap in knowledge in connecting the consequences of epilepsy-associated SCN2A (gene encoding for sodium ion channel Nav1.2) mutations, mutant channel dysfunction and epilepsy phenotype. This makes it challenging to discriminate between benign variants and pathogenic mutations from genetic screenings, which results in imprecise diagnosis and treatment of such individuals. My thesis project narrows this knowledge gap by examining the effects of Nav1.2 mutations on ion channel function and neuronal excitability using electrophysiological, pharmacological, and computational tools.

I’ve examined the functional and pharmacological properties of a recurrent SCN2A mutation and revealed that developmentally-regulated alternative splicing of SCN2A impacts the severity of mutant channel dysfunction. I’ve also demonstrated that the previously unrecognized enhancement of slow inactivation appears to be a major driver of the mutant channel’s loss-of-function phenotype. Through integrating a computational model of Nav1.2 into an induced pluripotent stem cell-derived neuron via dynamic-clamp electrophysiology, I’ve also demonstrated the ability of Nav1.2 to modulate neuronal firing with respect to its expression and voltage-dependent property perturbations. My hope is that these studies will contribute to drawing the line from genetic screenings, to channel dysfunction, to neuronal excitability and ultimately to clinical phenotype, which in turn will hopefully – eventually – inform the precise and effective diagnosis and treatment of SCN2A-epilepsy patients.

Please tell us about a defining moment in your education at Feinberg thus far.

In my third year as a graduate student, I attended a presentation by Dr. Timothy Errington titled 'Increasing Rigor and Reproducibility: Lessons Learned from the Reproducibility Project: Cancer Biology'. This talk coincided with a particularly challenging period of my research when results I observed were inconsistent with published studies and with preliminary studies conducted in my own thesis lab. It was challenging to identify and control for every variable — especially for the minute differences between individuals’ research techniques — that contributed to an observation, and the lack of detail in published experimental and analysis protocols made me skeptical of the validity of any studies I read. In his presentation, Dr. Errington acknowledged that there is essentially no such thing as exact replication and suggested complete transparency to qualify any reported experimental results. This concept should be intuitive and common practice in research, but it is not. This presentation significantly shaped my own emphasis on transparency in reporting experimental design and methods just as thoroughly as sharing results and conclusions of my studies.

What do you hope to do with your degree / what are your plans for post-graduation?

After completing my PhD, I plan to pursue a career in computational neuroscience or data science in industry. I wish to apply my interdisciplinary neuroscience training towards the treatment of neurological disease, ideally in the field of neural prosthetics or brain-computer interface technology.