Faculty Research Interests
The Howell lab studies how dysfunction in the Reelin-Dab1 signaling pathway influences neuronal migration disorders, autism and Alzheimer's disease. In particular, we are interested in the crosstalk between the Reelin-Dab1 pathway and other molecular pathways linked to these conditions. We use mouse and cell culture models, including patient-induced pluripotent stem cells, to study the effects of signaling aberrations in these diseases.
The Hu laboratory studies mechanisms of retinal degeneration in the blinding disease retinitis pigmentosa and of brain malformations in syndromic congenital muscular dystrophies associated with development delays and ocular abnormalities. We use the zebrafish and mouse to model these human disorders. Currently, we are developing experimental gene therapies using various animal models.
The Matthews lab studies the role of extracellular microenvironment in normal brain development and maturation, and its contribution to neural disorders and injury. Our lab is particularly interested in a substructure within the extracellular matrix called the perineuronal net. This structure is a key regulator of developmental plasticity and has been implicated in an array of neuropsychological and neurological disorders. The lab utilizes a combination of biochemical, neuroanatomical, and molecular approaches to understand the function of perineuronal nets and the neural extracellular matrix in both the normal and damaged brain.
The Middleton lab is focused on determining the biological bases of psychiatric and neurological disorders. We use high-throughput genetic, epigenetic, and functional genomic techniques with human subjects or animal and cellular models to identify molecular mechanisms linked to these disorders. We are particularly interested in autism, schizophrenia, ADHD, Parkinson's disease, alcohol abuse, and traumatic brain injury.
The Olson laboratory studies neurodevelopmental disorders that disrupt dendritic initiation and growth. The dendrite is a major component of the wiring of the brain, and disruptions of dendritic development are associated with profound intellectual disability and epilepsy. We use multiphoton microscopy and mouse disease models to examine how genetic mutations, early neural activity and environmental factors affect dendritic growth and brain structure.
The Pignoni lab focuses on the roles of transcription factors and signaling molecules in neurogenesis and eye development. We primarily use the Drosophila melanogaster as an in vivo model, as it provides us with an incomparable platform for genetic analyses. We also work in cell culture and in yeast to dissect protein function at a molecular level. Lastly, we rely on transcriptomics to understand gene networks. Genes we study are cause of congenital disorders in humans. Dr. Pignoni currently serves as the Interim Chair of Neuroscience & Physiology.
Modification of synaptic neurotransmission at glutamatergic synapses and activation of Ca2+-dependent second messenger systems contribute to the processes of learning and memory, neuronal survival and differentiation. These systems play important roles in the neuronal dysfunction that is observed following stroke and ischemia, focal epilepsies, and Alzheimer’s disease. The Vallano lab was previously focused on analysis of the expression and functional responsiveness of distinct excitatory amino acid receptors (NMDA subtypes), modulation of responses by Ca+2-dependent protein kinases, and examination of the roles of these receptors and kinases in neuronal survival and differentiation. *Note that I have transitioned from research to medical education and my laboratory is no longer operational. I am available to discuss these research ideas with interested students, staff, and colleagues.
The Viapiano laboratory studies the mechanisms by which the neural microenvironment contributes to brain cancer initiation and growth. In particular, we focus on extracellular matrix components that trigger pro-tumoral effects and are produced by cancer cells. We generate novel reagents to target these molecules in brain cancer and utilize patient-derived and organ-on-chip tumor models; mouse models of cancer; molecular and cellular techniques; and high-end genomic analyses of brain cancer datasets and biopsy samples to develop new diagnostic and therapeutic strategies.
The MiNDS lab uses quantitative molecular biology and neuroanatomical techniques in the postmortem human brain and in animal models to understand the biological basis of schizophrenia. In order to understand normal human development and aging, we chart molecular and cellular brain changes across the human life span, in humans from two months in age to 100 years. Using cellular neurobiology, histology, anatomical molecular mapping, transcriptomics, and quantitative molecular assays of proteins, metabolites and enzyme activity to analyze the human cortex and basal ganglia, we seek to uncover the underlying causes of schizophrenia and other disorders.
The Cognitive Neuroscience of Schizophrenia Laboratory aims to expose the relationships between thought impairment, genetic influence, and brain dysfunction in people with schizophrenia. Our translational research uses molecular findings from our collaborators to identify novel treatment targets. We combine brain imaging (MRI/fMRI/DTI), cognitive testing, genetic testing, and analysis of molecular biomarkers to validate and repurpose existing medications as adjunctive treatments in schizophrenia.
The Zhu lab is focused on characterizing processes of brain development using the Drosophila model. In type II neuroblast lineages, intermediate neural progenitors greatly expand production of neurons. By elucidating mechanisms underlying the proliferation and differentiation of the intermediate neural progenitor cells, we hope to gain mechanistic insights into the generation of brain complexity and brain tumor formation. In the mushroom body of the adult Drosophila brain, the mushroom body output neurons connect through their dendrites to specific axonal segments of mushroom body neurons. We use this model to clarify cellular and molecular mechanisms underlying subcellular-specific targeting of dendrites. Such subcellular specificity of synaptic connections has profound impact on neuronal activity and function.