Bshara Awwad, Ph.D.
Meet the Researcher
Awwad received his doctorate in neuroscience from the Hebrew University of Jerusalem. Prior to his research career, he worked for over a decade as a clinical audiologist in Israel. He is now a postdoctoral fellow at Mass Eye and Ear/Harvard Medical School. Awwad’s 2026 Emerging Research Grant is generously funded by Hyperacusis Research.
While the field had thoroughly mapped how the auditory system processes sound features, the affective dimensions of hearing loss remained largely unexamined at the circuit level. This was puzzling given the clear anatomical connection between auditory cortex and the amygdala, and the fact that many people with hearing loss develop severe responses to sound—anxiety, aversion, pain.
My mentor, knowing my clinical background working with hyperacusis patients, suggested we investigate whether and how the amygdala was affected after noise-induced hearing loss. It was, admittedly, venturing outside the traditional boundaries of auditory research. When I started recording from the amygdala after acoustic trauma, the findings were striking: persistent hyperactivity and a failure to distinguish between threatening and neutral sounds. The mice responded similarly to both, suggesting a circuit-level explanation for the generalized sound aversion I had seen clinically.
The project crystallized when we connected this to our lab’s work showing that 40 Hz stimulation of cortical inhibitory neurons produces sustained changes in sound processing. If the cortical-amygdala pathway drives hypersensitivity, modulating it might address both perceptual and affective aspects of hyperacusis—even when cochlear damage persists.
The turning point came during my clinical work as an audiologist. I had the privilege of improving the quality of life for hundreds of patients. However, I repeatedly encountered limitations in addressing their deeper questions about the mechanisms underlying hearing-related disorders—not just hearing loss, but tinnitus, hyperacusis, and conditions linked to auditory processing difficulties.
After years of this pattern, I realized that while I valued the clinical work, I wasn't satisfied simply managing symptoms without understanding underlying causes. Despite having an established career and stable position, the unanswered questions kept accumulating. It became clear that the work I found most meaningful—understanding why these disorders occur—required a fundamental shift toward research. The realization that I needed to pursue answers even if it meant starting over is what told me my career had to be in science.
Reading a 2010 Neuron paper from the lab of Dan Polley, Ph.D., during my clinical years demonstrated how early hearing loss induces persistent changes in cortical sound processing—it was a “bolt of lightning” moment. It showed me that labs were investigating these questions in animal models and confirmed my hunch that conditions like tinnitus and hyperacusis might reflect changes far beyond the cochlea, at levels my clinical tools couldn’t reach. That paper made joining the Polley lab my goal.
If I were not a research scientist, I would have become an archaeologist, which involves solving mysteries from incomplete evidence .
I have two hobbies that connect to research in opposite ways. I cook—which provides instant feedback compared to experiments. In the lab, I wait weeks to see if something worked; in the kitchen, I know in minutes whether I've ruined dinner. Both require precision and understanding how components interact, though burned garlic is more forgiving than a failed viral injection.
I also tend olive trees I planted years ago, which makes even my longest experiments feel quick. Waiting weeks for neural data seems reasonable when I'm simultaneously waiting years for olives. Both trees and research reward patience and careful observation, and both produce their best results when I embrace the unexpected—branches sometimes grow in surprising directions, just as in science, where sometimes the most interesting findings come from data that refuses to behave as predicted.
Together, these hobbies keep me balanced: cooking satisfies my need for immediate problem-solving, while the olive trees remind me that meaningful work unfolds over years, not weeks.
I distill my own arak, a traditional Middle Eastern anise-flavored spirit my grandfather used to make. The process is unforgiving—wrong temperature or timing and you get something closer to paint thinner than anything drinkable. I've had plenty of batches go wrong, but when it works, sharing a bottle I made from scratch feels like preserving something that could easily disappear across generations and geography.
In the future, I see myself running an independent lab investigating auditory processing and affective responses—keeping the questions broad since the clinical problems that drove me here are interconnected. The goal is building a research program that values unexpected results, mentors people from nontraditional backgrounds, and actually translates findings into useful interventions. The real measure of success won't be publications or funding—it'll be whether someone with hyperacusis benefits from what we discover.
The Research
Bshara Awwad, Ph.D. | Mass Eye and Ear
Auditory-limbic circuit dynamics as therapeutic targets in hyperacusis
Our research addresses a critical gap in understanding the neural basis of hyperacusis by focusing on brain circuits link the auditory and limbic systems. Previous work has established that cochlear damage leads to hyperexcitability throughout the central auditory pathway, but our approach uniquely focuses on the circuit-specific mechanisms that translate sensory hyperactivity into affective qualities akin to discomfort or even pain.
Specifically, we investigate how noise-induced hearing loss affects two parallel pathways to the lateral amygdala: the cortico-amygdalar (CAmy) and thalamo-amygdalar (TAmy) projections. This pathway-specific investigation represents a novel approach to understanding hyperacusis, as it targets the precise neural circuits that may mediate both the perceptual and affective components of this disorder.
Long-term goal: This research investigates why people with hearing loss sometimes develop hyperacusis—a condition where everyday sounds become overwhelmingly loud and can even cause physical pain. We're examining brain pathways that connect hearing centers to the amygdala, a region involved in evaluating affective sound qualities. Our specific aims are to: determine which brain circuits drive the heightened sound sensitivity and negative valence bias in hyperacusis; test whether targeted stimulation at 40 Hertz (Hz) can restore more normal sound processing; and explore whether measurable physiological responses, such as pupil changes, correlate with symptom severity.
Hyperacusis affects millions of people and currently has no approved treatments. This work may contribute to future therapeutic approaches in several ways: The findings suggest that interventions targeting central brain circuits could potentially help even when inner ear damage cannot be reversed—similar to approaches in chronic pain management that focus on the nervous system rather than the original injury site; the 40 Hz stimulation protocol showing sustained effects in our animal model could inform development of non-invasive stimulation approaches for human patients, though significant additional research would be needed to translate these findings to clinical practice.
Generously funded by Hyperacusis Research
