We are exploring whether anodal tDCS when administered in combination with spelling, naming, or working memory therapy can improve language performance of PPA and MCI participants at least in the short term more than behavioral therapy alone. We are also investigating whether and how tDCS alters the neuropeptide signature in participants with PPA and MCI. We use proton magnetic resonance spectroscopy (1H-MRS) to monitor neuropeptide concentrations at the areas of stimulation. We hypothesize that tDCS will stabilize the decline of specific neuropeptides, but only in those areas of the brain where tDCS effectively results in more efficient gains in language compared to language therapy alone (with sham tDCS). Study results may help optimize future intervention in individuals with PPA and MCI by providing treatment alternatives in a neurodegenerative condition with no proven effective treatment. A better understanding of the therapeutic and neuromodulatory effects of tDCS in PPA and MCI will offer insight into ways of impeding neurodegeneration that may improve quality of life for individuals with PPA and MCI and may provide insights into the mechanisms of this treatment for augmenting therapy for stroke as well.

The Seth Margolis Laboratory studies the signaling pathways that regulate synapse formation during normal brain development to try to understand how, when these pathways go awry, human cognitive disorders develop. We use Ephexin5 to study the molecular pathways that regulate restriction of excitatory synapse formation and their relevance to the pathophysiology of Angelman syndrome.

The mission of the Stroke Cognitive Outcomes and Recovery (S.C.O.R.E.) Lab is to enhance knowledge of brain mechanisms that allow people recover language, empathy, and other cognitive and communicative functions after stroke, and to improve ways to facilitate recovery of these functions after stroke. We also seek to improve the understanding of neurobiology of primary progressive aphasia., and how to enhance communication in people with this group of clinical syndromes.

The Systems Biology Lab applies methods of multiscale modeling to problems of cancer and cardiovascular disease, and examines the systems biology of angiogenesis, breast cancer and peripheral artery disease (PAD). Using coordinated computational and experimental approaches, the lab studies the mechanisms of breast cancer tumor growth and metastasis to find ways to inhibit those processes. We use bioinformatics to discover novel agents that affect angiogenesis and perform in vitro and in vivo experiments to test these predictions. In addition we study protein networks that determine processes of angiogenesis, arteriogenesis and inflammation in PAD. The lab also investigates drug repurposing for potential applications as stimulators of therapeutic angiogenesis, examines signal transduction pathways and builds 3D models of angiogenesis. The lab has discovered over a hundred novel anti-angiogenic peptides, and has undertaken in vitro and in vivo studies testing their activity under different conditions. We have investigated structure-activity relationship (SAR) doing point mutations and amino acid substitutions and constructed biomimetic peptides derived from their endogenous progenitors. They have demonstrated the efficacy of selected peptides in mouse models of breast, lung and brain cancers, and in age-related macular degeneration.

Dr. Raul Chavez-Valdez is an assistant professor in the Department of Pediatrics with great interest in the mechanisms of delayed injury and repair/regeneration in the developing neonatal brain following injury, specifically following hypoxic-ischemic encephalopathy (birth asphyxia). He collaborates with Dr. Frances Northington (Pediatrics) and Dr. Lee Martin (Pathology/Neuroscience) in unveiling the importance of programmed necrosis in the setting of brain injury induced by birth asphyxia. He is especially interested in the role of brain derived neurotrophic factor and neurotrophin-4 following birth asphyxia and the changes that may explain the suspected excitatory/ inhibitory (E/I) imbalance particularly in the hippocampus. His work is highly translational since delayed hippocampal injury due to E/I imbalance may explain memory deficits observed despite therapeutic hypothermia in neonates suffering birth asphyxia. All of these aspects of developmental neuroplasticity are the base of his Career Development Award (NIH/NINDS-K08 award) and applications to other agencies. Additionally, he is part of multiple clinical efforts as part of the Neuroscience Intensive Care Nursery (NICN). He has been a Sutland-Pakula Endowed Fellow of Neonatal Research since September 2013.

The Ronald Schnaar Lab is involved in the rapidly expanding field of glycobiology, which studies cell surface glycans, lectins, and their roles in cell physiology. Current projects in our lab study include (1) Glycans and glycan-binding proteins in inflammatory lung diseases, (2) Ganglioside function in the brain, and (3) HIV-Tat and HIV-associated neurocognitive disorders.