Vijaya Prakash Krishnan Muthaiah, Ph.D.

Meet the Researcher

Krishnan Muthaiah completed postdoctoral training in auditory neuroscience at the University at Buffalo, New York, and Purdue University, Indiana, after receiving his doctorate in molecular biology–anatomy from the University of Madras, India. He is an assistant professor in the department of rehabilitation sciences at the University at Buffalo. His 2019 Emerging Research Grant is generously funded by Royal Arch Research Assistance.

During my doctoral studies, I began to investigate the effects of neurotrauma-induced oxidative stress. During my postdoctoral training, I examined the effect of cell death in the auditory system. Though well studied in the peripheral auditory system (outer, middle, and inner ear), the effects of noise exposure on the central auditory system (from the brainstem to the brain) remain understudied, especially in blast noise exposure where both auditory and non-auditory structures in the brain are affected.

Hearing loss from sudden blasts differs from hearing loss from continuous noise as it is more likely to be accompanied by cochlear synaptopathy (a problem with nerve cell synapses), accelerated cognitive deficits, depression, anxiety, dementia, and brain atrophy. It has been well established that the enzyme PARP (poly ADP-ribose polymerase) is a key mediator of cell death and that it is overactivated by oxidative stress. My current work will examine the potential dampening of PARP using its inhibitor, 3-aminobenzamide.

My interest in science was sparked by a high school science fair competition and motivational support from my chemistry teacher, the first of several important mentors during my studies and career. As an undergraduate I read the book “Genes” by Benjamin Lewin, which inspired me to get my master’s in molecular biology. The unresolved mysteries of brain function led to my interest in neuroscience and, eventually, in the electrical properties of the nervous system.

I became aware of the emotional stress from hearing loss when I helped a fellow doctoral student collect blood samples from subjects with congenital hearing loss. Since I had studied neurotrauma, I began to look at acoustic trauma.

Biology is an amalgamation of physics, chemistry, and mathematics, so I have been studying instrumentation, statistics, and programming. This will help me reach a goal of investigating the distortion of neural information processing in post-impulse noise exposure. Eventually, I hope to become a tenured researcher with a focus on neurodegeneration due to neurotrauma and occupational hazards. I strongly believe the molecular targets that I am investigating may lead to clinical applications.

Vijaya Prakash Krishnan Muthaiah, Ph.D., is a Royal Arch Research Assistance award recipient. Hearing Health Foundation thanks the Royal Arch Masons for their ongoing commitment to research in the area of central auditory processing disorder.

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The Research

University at Buffalo, the State University of New York
Potential of inhibition of poly ADP-ribose polymerase as a therapeutic approach in blast-induced cochlear and brain injury

Many potential drugs in the preclinical phase for treating different types of noise-induced hearing loss (from blast and non-blast noise) revolve around targeting oxidative stress or interfering in the cell death cascade. Though noise-induced oxidative stress and cell death is well studied in the auditory periphery, the effects of noise exposure on the central auditory system remains understudied, especially in blast noise exposure where both auditory and non-auditory structures in the brain are affected. Impulsive noise (blast wave)-induced hearing loss is different from continuous noise exposure as it is more likely to be accompanied by accelerated cognitive deficits, depression, anxiety, dementia, and brain atrophy. It is well established that poly ADP-ribose polymerase (PARP) is a key mediator of cell death and it is overactivated by oxidative stress. Thus this project will explore the potential of PARP inhibition as a potential therapeutic approach for blast-induced cochlear and brain injury. The dampening of PARP overactivation by its inhibitor 3-aminobenzamide is expected to both mitigate blast noise-induced oxidative stress and to interfere with the cell death cascade, thereby reducing cell death in both the peripheral and central auditory system.

Long-term goal: To determine the mechanisms underlying both the peripheral and central aspects of blast-induced auditory neurodegeneration; and to identify and characterize potential therapeutic targets for manifestations of blast-induced traumatic brain injury, including hearing loss, cochlear synaptopathy, tinnitus, and associated deficits.