Human Brain and Cognition Lab

Acute lymphoblastic leukemia (ALL) is one of the most frequent types of cancer in children. Although childhood ALL is typically curable, the chemotherapeutic agents used in most treatment regimens are neurotoxic, and between 40-70% of children treated for ALL exhibit measurable deficits in cognitive functioning. However, the specific processing deficits contributing to poor cognitive functioning in survivors of childhood ALL and the implications for ongoing brain development are poorly understood.

We use a combination of behavioral, electrophysiological, and neuroimaging measures to demonstrate the impact on neurocognitive function, brain activity, and brain development following chemotherapy compared to healthy, matched controls. A preliminary study in our lab indicated deficiencies in all cognitive domains for survivors compared to age-matched controls (Brace et al. 2019). We are further investigating treatment-related effects on brain functions, identifying abnormal patterns of neural connectivity, and assessing the chronic effects of chemotherapy treatment on the development of cognitive skills in childhood survivors. Defining the loci of neurocognitive dysfunction caused by ALL treatment will guide the development of novel preventive, treatment, and intervention strategies.

Androgen deprivation therapy (ADT) is a hormone treatment for prostate cancer that reduces testosterone levels to slow tumor growth. However, it is theorized that treatment sometimes has the side effect of diminishing cognitive ability.

In our lab, we are using advanced brain imaging techniques to identify which cognitive abilities are most affected, in which individuals, and which specific brain regions or pathways are affected by ADT therapy. Our collaborators in Dr. Tiago Goncalves' lab are uncovering the mechanisms responsible for these changes in an animal model and testing intervention therapies that will lead to future clinical trials in humans.

The longer-term goal of our work is to help guide survivorship care by developing neurocognitive assessments and by making remedial interventions possible. Our results will also increase our understanding of the effects on brain functions associated with ADT therapy and facilitate our ability to make appropriate recommendations for improving cognition after therapy has ended.

The goal of our research is to determine the prevalence of central auditory processing disorder (CAPD) in children diagnosed with autism spectrum disorder (ASD) and to characterize the brain's response to speech and non-speech sounds in diagnosed children with and without CAPD. As many as 90% of people diagnosed with ASD have trouble with sensory processing. By doing this study, we hope to learn about the prevalence of auditory-specific deficits in people diagnosed with ASD, which is currently unknown. This knowledge will help us develop new diagnostic procedures and appropriate intervention strategies targeted at CAPD-specific deficits in children with ASD.

The long-term goal of this research is to improve communication ability by gaining a better understanding of specific complex central auditory functions in children diagnosed with autism. Currently, diagnosis of central auditory processing disorder (CAPD) is not part of standard clinical practice in diagnosing ASD. This project will diagnose CAPD in children previously diagnosed with autism and determine if children with ASD who also have CAPD have impaired for processing speech and other complex non-speech sounds, once peripheral functioning has been ruled out.

Tinnitus is defined by the perception of phantom sounds without an external source. It is described by patients as a bothersome "ringing," "buzzing," or "hissing" sound that only they can hear. Tinnitus is extremely common, affecting roughly 60 million people in the United States. It can also be debilitating, causing impairments in attention, communication, mental health, and overall quality of life. These outcomes drive substantial healthcare use, including frequent visits across primary care, audiology, otolaryngology, and mental-health services. In the United States alone, tinnitus-related healthcare spending reaches billions of dollars annually. It is also disproportionately effects veterans, and is the top compensated, service-related disability in the military, over twice as common as post-traumatic stress disorder. And yet, tinnitus still lacks effective treatments, largely because our scientific understanding of its underlying mechanisms is poor.

The biggest risk factor for tinnitus is hearing loss and 90% of people with tinnitus also have hearing loss. However, hearing loss is not the direct cause of tinnitus, and many people with hearing loss never develop tinnitus. Animal research suggests that tinnitus may be driven by brain hyperactivity that occurs in reaction to hearing loss, but neurophysiological proof of this in humans is lacking. Identifying human brain activity changes that are specific to tinnitus would help to understand the neural basis of phantom sound perception and would advance treatment and intervention strategies that could alter clinical practice.

The central goal of this research is to identify neural markers in humans that are specific to tinnitus. To accomplish these goals, we use advanced behavioral and electrophysiological techniques to measure and compare brain responses to sounds between patients with hearing loss and reported tinnitus and patients with hearing loss without reported tinnitus. Identifying specific neural markers for tinnitus would allow scientists and physicians to objectively measure disease activity, whereas currently we can only ask patients what their tinnitus sounds like and how it makes them feel. Additionally, these markers could be used to monitor how patients respond to treatment and to develop new, targeted therapies that address the root of the problem.