Kaushik Chanda is a postdoctoral researcher at The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology (Scripps Research). He studies how long non-coding RNAs drive structural plasticity and mitochondrial homeostasis, with implications for preserving cognitive function in conditions like Alzheimer’s disease and Huntington’s disease. In this Postdoc Portrait interview, he shares how he hopes to bridge several fields of biology and reframe the regulatory role of these non-coding nucleic acids.
Uncovering Non-coding RNA Functions in Synapses
Q | What drew you to circular RNAs?
I was drawn to the field of non-coding RNAs and neuronal biology by a fascination with how complex brain functions can be regulated by molecules once considered non-functional. During my research experience, I became particularly interested in the intersection of RNA biology, mitochondrial dynamics, and synaptic plasticity because these processes are central to learning, memory, and neurodegenerative disease. Despite major advances in neuroscience, many mechanisms underlying neuronal adaptability and vulnerability remain unresolved, especially the role of circular RNAs (circRNAs) in regulating cellular organelles and synaptic function.
My work on circRNAs emerged from this curiosity. Mitochondria are critical for neuronal energy demands and synaptic remodeling, yet little is known about how circRNAs influence mitochondrial behavior in neurons. The possibility that a stable, brain-enriched circRNA could directly modulate mitochondrial dynamics and neuronal plasticity opened an exciting and largely unexplored area of research. I am motivated by the opportunity to uncover new biological mechanisms that could ultimately contribute to therapies or biomarkers for neurological disorders.
Q | What scientific problem are you trying to solve?
CircRNAs are highly stable and abundant in neurons, yet the biological functions of most brain-enriched circRNAs remain unknown. Neurons rely heavily on precise mitochondrial transport, morphology, and bioenergetic balance to support synaptic plasticity, learning, and memory. However, the molecular mechanisms linking non-coding RNAs to mitochondrial behavior in neurons are poorly understood. My research focuses on understanding how nuclear encoded mitochondrial circRNAs regulate neuronal and synaptic function through control of mitochondrial dynamics and local energy homeostasis.
I aim to solve the fundamental problem of how circRNA contributes to neuronal health and plasticity, and whether their deregulation leads to synaptic dysfunction and neurodegeneration. Using neuronal models, biochemical assays, live-cell imaging, and functional studies, I investigate how circRNA influences mitochondrial stability, trafficking, and activity-dependent remodeling at synapses. This work could uncover a previously unrecognized layer of RNA-mediated mitochondrial regulation in the nervous system and identify circRNA as a potential therapeutic target or biomarker for neurological disorders associated with mitochondrial dysfunction.
Target-Based Drug Discovery for Neurodegeneration
Q | What have you learned from studying circRNA that you didn’t expect?
One of the most unexpected things I learned from studying circRNA was how strongly mitochondrial behavior is linked to rapid synaptic remodeling in neurons. I initially approached circRNAs as gene regulatory molecules that would primarily influence transcriptional or post-transcriptional pathways. However, during my experiments, it became clear that altering circRNA levels could quickly affect mitochondrial stability, distribution, and dynamics within dendrites, ultimately influencing spine plasticity. This revealed a much more immediate and functional connection between non-coding RNAs and neuronal energetics than I had anticipated.
Another surprising insight was the versatility of circRNAs themselves. Traditionally viewed as relatively passive regulators or microRNA sponges, circRNAs may play far more active roles in coordinating organelle function and cellular responses to neuronal activity. This shifted the way I think about RNA biology—not as isolated layers of regulation, but as integrated components of cellular architecture and signaling. The project taught me the importance of exploring unconventional hypotheses, especially in fields where many fundamental mechanisms remain unknown.
Q | If your research succeeds, what could it change for science or society?
This work could fundamentally expand our understanding of how non-coding RNAs regulate neuronal function and mitochondrial biology. While circRNAs are abundant in the brain, their physiological roles remain largely unexplored. Demonstrating that a circRNA actively controls mitochondrial dynamics and synaptic plasticity would uncover a new layer of gene regulation that links RNA biology directly to neuronal energy homeostasis and brain function. This could have important implications for diseases where mitochondrial dysfunction and synaptic degeneration are central features, including Alzheimer’s disease, amyotrophic lateral sclerosis, Parkinson’s disease, and other neurodegenerative disorders. By identifying circRNA-mediated pathways, the research may reveal novel therapeutic targets that can stabilize neuronal health or improve synaptic resilience. In the long term, circRNAs could also serve as minimally invasive biomarkers because of their remarkable stability in biological fluids. More broadly, this work could shift how scientists think about “non-coding” regions of the genome, highlighting that these RNAs are not passive byproducts, but active regulators of cellular organization, communication, and adaptation in the nervous system.
Q | What question are you most excited to answer next?
I want to know how circRNA mechanistically communicates with mitochondria to regulate synaptic plasticity. While we are beginning to observe clear effects on mitochondrial stability and neuronal remodeling, the precise molecular pathway remains unknown. I am particularly interested in determining whether this circRNA acts through specific RNA-binding proteins, microRNA networks, or direct interactions with mitochondrial transport and dynamics machinery such as kinesins and fission-fusion regulators. I am also excited to explore whether the circRNA functions as an activity-dependent regulator during learning-like neuronal stimulation and whether its dysregulation contributes to neurodegenerative disease progression. Another important direction is investigating whether mitochondrial-associated circRNAs can be detected in extracellular vesicles or blood, potentially serving as biomarkers for neurological disorders. Answering these questions could bridge several fields—RNA biology, mitochondrial dynamics, and neuroscience—and help define a broader principle of how non-coding RNAs coordinate cellular energetics with synaptic adaptation. The possibility of uncovering an entirely new regulatory mechanism is what motivates me most.
Responses have been edited for length and clarity.
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