Neuroscience

My research program is centered on investigating the neurobiology of healthy language system, and changes in cognitive and language processing associated with stroke and neurological disorders. My interests include incorporating cognitive measures and multimodal neuroimaging methods, with a goal to understand the relationship between language and other aspects of cognition, as well as the neural dynamics related to brain damage, resilience, and recovery. My research efforts are directed towards identifying factors which affect language comprehension and production, and how these change with development and are influenced by aging, stroke, brain injury, and neurodegenerative disorders, including Primary Progressive Aphasia (PPA) and Alzheimer’s disease (AD). I study language processing at the multiple levels, using behavioral experiments and both structural (DTI, lesion-symptom mapping, voxel-based morphometry) and functional neuroimaging (fMRI, EEG, MEG). In addition, I am interested in neuroplasticity and application of noninvasive brain stimulation techniques (e.g., TMS, tDCS) to the treatment of aphasia and dementia. The long-term goal of my research is to understand the cognitive and neural processes that support recovery of cognitive and language functions after stroke. Keywords: stroke, aphasia, dementia, MRI, EEG, Language

Charles Higgins, PhD, is an Associate Professor in the Department of Neuroscience with a dual appointment in Electrical Engineering at the University of Arizona where he is also leader of the Higgins Lab. Though he started his career as an electrical engineer, his fascination with the natural world has led him to study insect vision and visual processing, while also trying to meld together the worlds of robotics and biology. His research ranges from software simulations of brain circuits to interfacing live insect brains with robots, but his driving interest continues to be building truly intelligent machines.Dr. Higgins’ lab conducts research in areas that vary from computational neuroscience to biologically-inspired engineering. The unifying goal of all these projects is to understand the representations and computational architectures used by biological systems. These projects are conducted in close collaboration with neurobiology laboratories that perform anatomical, electrophysiological, and histological studies, mostly in insects.More than three years ago he captured news headlines when he and his lab team demonstrated a robot they built which was guided by the brain and eyes of a moth. The moth, immobilized inside a plastic tube, was mounted on a 6-inch-tall wheeled robot. When the moth moved its eyes to the right, the robot turned in that direction, proving brain-machine interaction. While the demonstration was effective, Charles soon went to work to overcome the difficulty the methodology presented in keeping the electrodes attached to the brain of the moth while the robot was in motion. This has led him to focus his work on another insect species.

Michael Hammer is a Research Scientist in the Division of Biotechnology at the University of Arizona with appointments in the Department of Neurology, Ecology and Evolutionary Biology, Bio5, the School of Anthropology, the University of Arizona Cancer Center, and the Steele Children's Research Center. Currently Dr. Hammer is interested in the use of the latest DNA sequencing technology to infer the underlying genetic architecture of neurodevelopmental diseases. Since 1991 Dr. Hammer has directed of the University of Arizona Genetics Core (UAGC), a facility that provides training and molecular biology services to University and biotechnology communities at large. After receiving his Ph.D. in Genetics at the University of California at Berkeley in 1984, he performed post-doctoral research at Princeton and Harvard. Over the past two decades, Dr. Hammer has headed a productive research lab in human evolutionary genetics, resulting in over 100 published articles documenting the African origin of human diversity, interbreeding between modern humans and archaic forms of the genus Homo, and genome diversity in the great apes. His lab and the UAGC were early adopters of next generation sequencing (NGS) technology and the application of whole genome analysis in humans, and his lab has been a key player in the Gibbon and Baboon Genome Projects, as well as a consortium that has analyzed the genomes of over 100 Great Apes (GAPE Project). In the past 3 years, Dr. Hammer's research team has succesfully employed NGS methods to identify molecular lesions causing neurodevelopmental disorders in undiagnosed children. This has led to the publication of articles identifying pathogenic variants associated with early onset epileptic encephalopathies. His lab is also currently pursuing studies to identify modifier genes that alter the expression of major genes and how they contribute to phenotypic heterogeneity in Mendelian disorders.

My research interests are broadly focused on understanding the reciprocal relations of self and memory. How does the self influence learning and memory retrieval? How does memory contribute to one's sense of self? Uncovering the ways in which the self and memory interact may advance understanding of identity, elucidate the conditions and experiences that modify the self, and inspire clinical interventions that improve quality of life and wellbeing for people who have neurological or mental health conditions. Ongoing projects are investigating how to improve memory through self-referential encoding strategies in individuals with traumatic brain injury and other neuropsychological conditions. My current research also is investigating how individuals with amnesia (a profound learning and memory impairment) construct a sense of self and experience a sense of continuity in life.

The broad goal of my research is to understand the neural basis of emotion and social behavior in non-human primates. Our laboratory pioneered multichannel neural recordings from the amygdala of monkeys engaged in naturalistic social interactions. Neural activity was monitored simultaneously with cardiovascular and other autonomic parameters of emotion to capture unique, coordinated brain-body states. These states, and the transitions between them, are the neural underpinnings of our emotional experiences and the memory thereof. I bring to BIO5 expertise from a broad and diverse range of sources. I earned a medical in Romania in 1988, followed by postgraduate training in neurosurgery, and a Ph.D. in Neuroscience in 1996 at the University of Arizona. As a student, I explored the neural dynamics of spatial learning and memory in rats and determine the interaction of multiple spatial reference frames during navigation. I completed by postdoctoral studies at the UC Davis in primate socio-emotional behavior and the neurophysiological basis of communication with facial expressions. While at Davis, I received a K01 career development award that allowed me to assemble the largest existent annotated video library of macaque social behavior. I used this library to probe the behavioral and neural events that are the basic building blocks of social behavior (e.g., eye contact, the reciprocation of facial expressions, and gaze following). We discovered a specialized class of cell in the monkey brain that are active exclusively in the context of natural social behaviors and respond selectively to eye contact. We have developed techniques of precisely targeted bilateral microinjections in the primate brain and implemented successfully neural recording and parallel with microinjections of drugs and hormones. Currently we are testing the effect of various drugs in the activity of eye cells in the amygdala.

Fabian-Xosé Fernandez, PhD, Departments of Psychology and Neurology, McKnight Brain InstituteCircadian timekeeping is fundamental to human health. Unfortunately, under many clinical circumstances, the temporal organization of our minds and bodies can stray slowly from the Universal Time (UT) that is set with the Earth’s rotation. This disorganization has been linked to progression of several age-related and psychiatric diseases. Non-invasive phototherapy has the potential to improve disease outcomes, but the information that the brain’s clock tracks in twilight (or any electric light signal) to assure that a person entrains their sleep-wake cycles to the outside world is not understood. The central theme of my research program is to fill in this blank and to usher in an era where therapeutically relevant “high-precision” light administration protocols are institutionalized at the level of the American Medical and Psychiatric Associations to change the standard of care for a wide variety of conditions that impair quality of life. Of the conditions my lab is currently studying, we are particularly interested in how chronic and quick, sequenced light exposure can be designed to: 1. promote normal healthy aging and 2. strengthen adaptive cognitive/emotional responses to being awake in the middle of the night (12-6AM), a key interval of the 24-h cycle that we have associated with increased suicidal ideation and mortality. Our circadian work on suicide is done in very close partnership with the University of Arizona Sleep Health and Research Program directed by Dr. Michael A. Grandner.

Lisa Elfring is an Associate Specialist in the Department of Molecular and Cellular Biology and currently serves as Associate Vice Provost for Instruction and Assessment. In this administrative role, she leads the Office of Instruction and Assessment (OIA), which supports teaching and learning across campus. The office supports technology-enabled teaching (D2L, Panopto, Adobe Connect, VoiceThread); provides professional development and courses on evidence-based teaching for all UA instructors; produces media products (web pages, videos) that support instructors in their teaching; helps departments to carry out assessment of learning outcomes; and helps to connect instructors across departmental and college boundaries. Dr. Elfring is currently involved in two teaching-related research projects. In one, she and her collaborators are investigating a model to train instructors in large, collaborative STEM classes to utilize a team of graduate and undergraduates to improve student learning. In the other, the team is investigating the effects on students on creating and improving models in biological systems, in the context of an Introductory Biology lab course. Both projects are funded by awards from the National Science Foundation. Dr. Elfring's teaching experiences range from large courses in introductory cell/molecular biology and cell biology, to courses focusing on helping undergraduate students to prepare for doing laboratory research. Her research interests are integrated with her teaching role. She is interested in process of systemic change in educational systems, and particularly in how the university can promote the adoption, use, and assessment of research-based teaching strategies across the entire range of STEM (science, technology, engineering, and math) courses. In biology education, she has been involved in research on how students come to make sense of the key biological concept that genes code for RNAs which (mostly) encode proteins to form the structural and catalytic molecules of the cell, a process that is termed the central dogma of molecular biology. She and her collaborators were involved in efforts to introduce more quantitative problem-solving work in the Introductory Biology course and across the undergraduate life-sciences curriculum. Her undergraduate, graduate, and post-doctoral training is in molecular, cell, and developmental biology; she has done research using humans, mice, and fruit flies as experimental systems to investigate embryonic development and cancer. Keywords: Biology education, Faculty professional development

The broad goal of research in our laboratory is to understand how inhibitory inputs influence neuronal signaling and sensory signal processing in the healthy and diabetic retina. Neurons in the brain receive inputs that are both excitatory, increasing neural activity, and inhibitory, decreasing neural activity. Inhibitory and excitatory inputs to neurons must be properly balanced and timed for correct neural signaling to occur. To study sensory inhibition we use the retina, a unique preparation which can be removed intact and can be activated physiologically, with light, in vitro. Thus using the retina as a model system, we can study how inhibitory synaptic physiology influences inhibition in visual processing. This intact system also allows us to determine the mechanisms of retinal damage in early diabetes. Keywords: neuroscience, diabetes, vision, electrophysiology, light

Feeding and anxiety are two conserved behaviors critical to survival and health in all mammals. These two behaviors are interacting with each other in health and disease. Patients with abnormal feeding behaviors during eating disorders or obesity are usually associated with anxiety and depression. These two behaviors are controlled by distinct neural circuits distributed across multiple brain regions. However, whether the neural circuits underlying these two behaviors have overlap or interactions is still unknown. The lab of Dr. Haijiang Cai studies the neural circuits of animal behaviors, with a focus on understanding how the neural circuits regulate feeding and emotional behaviors. The recent work from his lab identified a specific population of neurons in the amygdala, a brain region well known for emotion control, also plays important roles in appetite control. His lab is using state-of-the-art optogenetics, chemogenetics, electrophysiology and in vivo microendoscope calcium imaging to dissect the neural circuits. This research will help understand how feeding and anxiety interact with each other, and provide new insight in developing drugs to treat eating and emotional disorders with fewer side effect. Keywords: Neural circuits, Behavior, Feeding, Anxiety

My work investigates the molecular mechanisms of axon degeneration, a molecular program triggered by toxic, metabolic, or traumatic stress to the axonal compartment of neurons. I use both fruit fly and mouse tools to ask questions about genes involved in axon degeneration and to place these genes in the context of pathways required for axon and synapse maintenance in the face of insults. I have discovered a number of axon degeneration mediators, including MORN4 and TMEM184b as well as others, and am currently following up on their roles within neurons during normal neuronal functioning and in the context of neurodegenerative disorders such as ALS and Alzheimer’s Disease. Keywords: Neurodegeneration, Neurogenetics, Behavior