Ph.D. Thesis Mentors

Associate Professor, Pharmacology and Physiology
Ahern Lab
Office: Med-Dent SW401
Lab: Med-Dent SW402
Education: BSc (Hons), 1990, LL. B., 1991, University of Canterbury (New Zealand); PhD, 1996, Australian National University (Australia)
Current Research: How do cells detect changes in the external or extracellular environment? We are interested in the fundamental mechanisms that allow cells to sense diverse chemical or physical stimuli. Our focus is a class of membrane ion channels called “Transient Receptor Potential” (TRP) channels. We also explore novel ligand signaling at G-protein coupled receptors both in neurons and immune cells. We use a combination of electrophysiological, cell imaging, genetic and biochemical techniques, and where possible, appropriate animal models.

Tinatin I. Brelidze

Associate Professor, Pharmacology and Physiology
Brelidze Lab
(202) 687-6178
Office: Med-Dent SE406
Lab: Med-Dent SE406
Education: Diploma in Physics (Hons), Tbilisi State University (Georgia), 1996; Ph.D. Physiology & Biophysics, University of Miami, 2003
Current Research: Ion channels are integral membrane proteins that regulate the passage of ions through cell membranes.  Ion channels are essential for physiological function of living cells and abnormalities in ion channel function or expression pattern are often linked to inherited or acquired diseases. The research in my laboratory is focused on studies of mechanisms responsible for opening and closing of ion channels, identification of novel ion channel regulators and investigation of therapeutic potential of ion channel regulators.  In our studies we use a variety of methods, including electrophysiology, biochemistry techniques, fluorescence-based methods, and zebrafish and rodent animal models.

Katherine Conant

Associate Professor, Neuroscience
Conant Lab (new window)
(202) 687-
Office: Research Building EP-16
Education: M.D. Boston University School of Medicine
Current Research: Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that can be released and/or activated in a neuronal activity dependent manner. MMP expression and activity can also be dramatically upregulated with injury, including that mediated by infection or hypoxia.

While recent studies suggest that MMPs play a role in normal learning and memory, the mechanisms by which they do so are not completely understood. Our work is focused on the mechanisms by which MMPs influence neuronal and synaptic structure and function. We are particularly interested in their ability to cleave specific synaptic adhesion molecules, and to stimulate signaling by G protein coupled protease activated receptors. We are also interested MMP dependent cleavage of perineuronal net components as a means to influence neuronal population dynamics. These lines of research have implications for the study of depression as well as neuroinflammation.

We collaborate with several investigators at Georgetown including Jian-Young Wu, Stefano Vicini, John Partridge, Ken Kellar, Sonia Villapol, Rhonda Dzakpasu, and Kathleen Maguire-Zeiss.

Rhonda Dzakpasu

Associate Professor, Physics and Pharmacology
Neural Dynamics Lab (new window)
(202) 687-4918
Office: Med-Dent C405
Lab: Med-Dent C405
Education: University of Michigan, Ph.D., 2003 
Current Research: We use arrays of extracellular multi-electrodes to record and stimulate electrical activity from cultured neural circuits as well as from acute neural slices. We modulate network rhythmicity by manipulating the balance between excitation and inhibition to investigate the principles by which neurons interact. What is the causal role of emergent coherent activity for neuronal communication?

Patrick A. Forcelli

Director, PhD in Pharmacology & Physiology;
Associate Professor, Pharmacology & Physiology
Website (new window)
Office: NRB W214
Education: Ph.D. (Neuroscience), Georgetown University, 2011
Current Research:  Research in the laboratory focuses on the neural circuitry underlying seizure propagation, complex behaviors, and the pharmacological treatment of neonatal seizures. We use a combination of approaches ranging from biochemistry and histology to neurophysiology (in slice and in intact animals) to behavioral monitoring and circuit manipulation (pharmacological, optogenetic, chemogenetic) to neuroimaging.

Robert Glazer

Professor, Oncology
Glazer Lab
(202) 687-8324
Office: Research Bldg W318
Lab: Research Bldg W317, W321, W324
Education: Ph.D., Indiana University, 1970
Current Research: Role of the nuclear receptor PPARdelta, a ligand-dependent transcription factor, involved in oxidative metabolism and tumorigenesis. We examine the oncogenic and metabolomic signaling pathways in a mouse model and in tumor cell lines. We established a PPARdelta-dependent gastric cancer model sensitive to a PPARdelta suicide inhibitor. Other studies concern the role of stem cell antigen-1 (Sca-1) in mammary tumorigenesis. Sca-1 is a marker of stem and early progenitor cells, but the function has remained a mystery. We have found that Sca-1 inhibits TGF- signaling through a unique pathway that activates Smad3. Loss of Sca-1 also reactivates other tumor suppressor genes, such as PTEN and PPARgamma. Thus, our current research focuses on the inter-relationships between oncogenic and stem cell pathways and their roles in modulating tumorigenesis.

Nady Golestaneh

Associate Professor, Opthalmology, Neurology, & Biochemistry
PubMed search for publications (new window)
(202) 687-8324
Office: Med/Dent NE203
Current Research: My research focuses on age-related macular degeneration (AMD). AMD is a devastating neurodegenerative disease and the leading cause of blindness in the elderly. More than 11 million Americans over the age of 50 are affected by AMD, and with an aging population, this number is expected to double by 2050. My research program involves three complementary areas in AMD, 1) investigating the underlying mechanism of AMD using adult stem cells and In vitro disease modeling, 2) establishment of new animal models to study AMD and test novel drugs in vivo, and 3) investigating how aging mechanisms can induce retinal degeneration and AMD.

Jeffrey K. Huang

Assistant Professor, Biology
Lab Website (new window)
(202) 687-1741
Office: Regents 406
Lab: Regents 411
Education: Ph.D., Mount Sinai School of Medicine
Current Research: My lab is interested in the biology and pathology of glial cells. We focus on oligodendrocytes, a type of glia, whose cellular processes engage with and enwrap CNS axons, and form the lipid-rich myelin membranes required for rapid, saltatory conduction. Myelin destruction in diseases such as multiple sclerosis impairs axonal conduction and results in progressive axonal degeneration. We are currently investigating the mechanisms by which oligodendrocytes interact and communicate with axons, and how their interactions might promote axonal integrity and survival. We are also investigating the mechanism of myelin regeneration, with a focus on how oligodendrocytes regenerate from endogenous neural progenitor cells to replace myelin during homeostatic turnover or after demyelination. We use primary oligodendrocyte/neuron co-cultures, transgenic mice, and models of experimental CNS injury and demyelination, combined with molecular biology and imaging tools to address these questions.

Ken Kellar

Professor, Pharmacology and Physiology
Lab Website
(202) 687-1032
Office: Medical Dental Bldg SE402
Lab: Medical Dental Bldg NE416-420
Education: Ph.D., Pharmacology, The Ohio State University, 1974
Current Research: My laboratory studies the subunit composition, pharmacological properties and regulation of neuronal nicotinic receptors. We are particularly interested in understanding the importance of desensitization of these receptors and the mechanisms by which chronic exposure to nicotine increases these receptors in brain.

Kathy Maguire-Zeiss

Associate Professor, Neuroscience
Maguire-Zeiss Lab (new window)
(202) 687-2791
Office: NRB EP08
Lab: NRB EP08
Education: Albright College, BS, 1981; Pennsylvania State University College of Medicine, Ph.D., 1987
Current Research: My laboratory is focused on understanding the mechanisms involved in age-related progressive neurodegenerative diseases. Specifically, we are investigating why the nigrostriatal pathway degenerates in Parkinson’s disease (PD). Although the cause of PD is unknown we believe that the etiology involves both genetic changes and environmental toxicants. We are currently following several lines of investigation including the role of increased oxidative stress, protein misfolding and inflammation using mouse transgenic and toxicant models as well as cell culture technologies. Thus far we have shown that one protein known to be involved in Parkinson’s disease, α-synuclein, can increase oxidative stress and proinflammatory molecules suggesting that these molecular events are important early in this disease. We hope our studies will help us to better understand how inflammation is involved early in PD. Finally, our goal is to develop novel therapies for PD.

Professor, Pharmacology
(202) 687-0224
Office: NRB, W209B
Lab: DCM
Education: BA, MA Charles University Prague, Czech Republic; Ph.D. (1986) Czechoslovak Academy Sciences, Prague, Czech Republic
Current Research: Neural substrates of social and emotional behavior; the role of the amygdala and orbitofrontal cortex in processing reward; medial temporal lobe structures (hippocampus, perirhinal cortex) and cognitive functions (object recognition and spatial memory); amygdala and midbrain (superior colliculus) interactions; autism, PTSD; reversible pharmacological manipulations of discrete brain structures, systemic drug effects.

Italo Mocchetti

Professor, Neuroscience, secondary appointment in Pharmacology
Dr. Mocchetti’s homepage
Office: NRB, WP13
Lab: NRB, EG19
Education: Ph.D., University of Milan, Italy, 1982
Current Research: Neurotrophic factors influence axon and dendrite growth, synaptic plasticity and neurogenesis, and the interaction of neurons with glial cells. They play critical roles in preventing neurological diseases including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, stroke and epilepsy, but they can also promote neuronal apoptosis. Our laboratory has recently demonstrated that the neurotrophin brain-derived neurotrophic factor (BDNF) modulates the expression and function of chemokine receptors that contribute to AIDS dementia complex. We envision this research as catalyzing important new efforts to translate the basic science of the neurotrophins into effective new treatments for neurodegenerative diseases.

Sreejith Nair

Assistant Professor, Oncology and Lombardi Comprehensive Cancer Center
Office: NRB E308
Education: Ph.D. (Molecular Biology), UT Health Science Center San Antonio, 2012
More than 98% of the human genome does not code for any proteins, but they play crucial roles in normal physiology and diseases by controlling gene expression. The regulatory functions of the “non-coding genome” are primarily attributed to the RNAs produced from these regions (non-coding RNAs) and also gene regulation mediated by transcriptional enhancers. The mechanism of regulatory communication between protein-coding and non-coding genomic regions is largely unknown. In the lab, we use cutting-edge molecular biology, genomics, biophysics, and microscopy tools to study the mechanism of gene regulation by non-coding genomic elements. Our recent findings support the view that acute signaling events lead to the assembly of transcription complexes as liquid-like membraneless structures known as biomolecular condensates. Transcriptional condensates are RNA-protein complexes that have been shown to control gene expression, organize chromatin structure, and facilitate the recruitment of several anticancer drugs to the chromatin. We explore the biological and pharmacological role of these assemblies in vitro and in vivo by examining the biochemistry and biophysics of proteins and RNAs involved in the process.

Alexey Ostroumov

Assistant Professor, Pharmacology and Physiology
Website (new window)
PubMed search for publications (new window)
Office: W224A NRB
Education: PhD, International School for Advanced Studies (SISSA, Italy), 2010
Current Research: Our main goal is to understand the causal mechanisms, by which modifications in synaptic plasticity contribute to neural circuit remodeling and aberrant behaviors associated with neuropsychiatric disorders. To this end, we combine slice and in vivo neurophysiology with viral-genetic and behavioral approaches.

Daniel Pak

Professor, Pharmacology and Physiology
Molecular Neurobiology of Memory [mNeMe]
(202) 687-8750
Office: SW407 Med/Dent
Lab: SW406 Med/Dent
Education: Harvard University, B.A., 1991; University of California at Berkeley, PhD, 1996
Current Research: My laboratory is interested in the molecular changes that occur at CNS synapses in response to experience. We utilize a combination of approaches ranging from molecular biology and biochemistry to cell biology, imaging, and mouse genetics to address three major questions: 1) how do neurons encode long-term storage of information? 2) how do neurons maintain stability of function by homeostatic synaptic plasticity mechanisms? and 3) how does failure of these mechanisms contribute to neurological and neurodegenerative disorders?

G. William Rebeck

Professor, Department of Neuroscience
Rebeck Lab (new window)
(202) 687-1534
Office: NRB WP-10
Lab: NRB WP-04; NRB WP-27
Education: A.B. (Cornell University 1982); Ph.D. (Harvard University, 1991)
Current Research: I have been studying the effect of APOE on Alzheimer’s disease pathogenesis since 1993. APOE is the strongest genetic risk factor for Alzheimer’s disease, with the APOE4 allele increasing the risk of Alzheimer’s disease by over three-fold. We study the role of apoE in synapse formation and neuronal signaling, and its effects on glial activation using cell lines and primary cell culture systems. In particular, we focus on the family of cell surface apoE receptors, which play important roles in cholesterol regulation, neuronal migration in development, and cell signaling. We also study APOE knock-in mice, which express the human APOE alleles under the endogenous mouse APOE promoter. We have found that the APOE4 mice have reduced neuronal complexity and increased sensitivity to glial activation These effects of APOE occur in the absence of Alzheimer’s disease pathological changes, suggesting that APOE also affects normal brain patterns and functions.

Anna Tate Riegel

Professor, Departments of Oncology & Pharmacology
Riegel Lab (new window)
(202) 687-1534
Office: NRB E307A
Lab: NRB E307
Education: Ph.D. (Oncology) University of Wisconsin
Current Research: Dr Riegel’s research is focused on the role and regulation of nuclear receptor coactivators in epigenetic changes that drive breast cancer progression. The long-term goal of her research is to understand how epigenetic signals enhance tumor cell / stromal and immune interactions and ultimately to determine ways that this cross talk could be interrupted therapeutically. In one project her lab is investigating the mechanism that the cell cycle regulator CDK4/6 uses to inhibit progression of early stage breast cancer. In a second project her lab is focused on how the nuclear receptor coactivator AIB1 (amplified in breast cancer 1) and its more active oncogenic isoform 4, as well as the co-repressor ANCO1 drive the development of breast cancer. We have determined that these coregulators exist in chromatin as a complex that results in transcriptional repression, via epigenetic regulation of pro-oncogenic gene expression. We are currently investigating the regulation of this epigenetic event and if therapeutic intervention with epigenetic regulators can alter cancer progression in vivo.

Niaz Sahibzada

Associate Professor, Department of Pharmacology & Physiology
(202) 687-1500
Office: 410 Med/Dent
Lab: 412 Med/Dent
Education: Ph.D. (Neuroscience) University of Sheffield, England 1990
Current Research: The emphasis of research in my laboratory is on understanding the brain neurocircuits that regulate the function of the upper gastrointestinal tract such as those that control gastric tone and motility. To this end, we employ varied approaches that include microinjection of chemical substances in the brain, recordings of end organ function, patch-clamp electrophysiology in brain slices and neuroanatomical tract tracing.

Niaz Sahibzada

Click for a complete list of published work in MyBiblography. (new window)

Professor, Division of Nephrology & Hypertension, Department of Medicine
Website (new window)
(202) 687-3010
Office: 232 Bldg D
Education: Ph.D. (Biochemistry), University of Maryland, 1987
Current Research: 1. Angiotensin receptor signaling and trafficking: The angiotensin type 1 receptor is a peptide hormone G protein-coupled receptor that is widely targeted to treat hypertension. We previously discovered that RNA binding proteins regulate the function of the rat type 1a receptor (AT1aR) by selectively binding within exon 2 of the receptor 5′-leader sequence and that this translational regulation is mediated by a short open reading frame in exon 2. More recently, this research direction has led to the exciting discovery of a seven amino acid peptide (PEP7) encoded within a short open reading frame in exon 2, which is a selective inhibitor of AT1aR signaling; PEP7 inhibits the Erk1/2 but not the classic inositol trisphosphate pathway. PEP7 may also contribute to age-related impairments in urine-concentrating mechanisms and modulates AT1aR trafficking. We study AT1aR signal transduction by conducting enzyme and radioligand binding assays as well as by measuring signaling molecules on Western blots. AT1aR trafficking is investigated using live cell imaging and confocal microscopy in cells transfected with wildtype and site-directed mutants of the AT1aR.
2. Immune system and hypertension: Our laboratory investigates T cell mechanisms underlying the susceptibility and resilience to developing hypertension. We have found that male T cells exacerbate hypertension in an induced model of hypertension in the male mouse but are unable to achieve the same magnitude of hypertension in the female. Furthermore, female T cells are not able to contribute to hypertension in the male mouse. These findings indicate biological sex is a critical determinant in T cell differentiation and/or function. We are currently investigating how gonadal hormones and sex chromosomes affect sex-specific T cell function in models of hypertension and associated vascular and renal disease. We study blood pressure and heart rate by radiotelemetry in conscious mice and rats. T cell expression and function is assessed by flow cytometry and cytokine production in the Dahl rat model, gene-specific knockout mice and the four core genotype mouse model that enables separation of sex chromosomes from gonadal hormones.
3. Ovarian hormone loss, physical activity, blood pressure and cognition: Recent laboratory studies focus on the physical and cognitive effects of bilateral oophorectomy prior to the age of natural menopause. The resulting sudden ovarian hormone loss accelerates the age-associated development of hypertension and cognitive decline. We are also studying how physical activity and blood pressure can modulate cognitive decline in this model. Physical activity is controlled using voluntary and forced running wheels. Cognition is assessed by a 12 arm radial maze and novel object recognition tests. In addition, we are studying these questions through human subject research using wireless technology, home blood pressure, heart rate and pulse wave velocity monitors in conjunction with consumer activity trackers.

Yuichiro Suzuki

Professor, Pharmacology & Physiology
Homepage (new window)
(202) 687-8090
Office: NW402a Med/Dent
Lab: NW403 Med/Dent
Education: PhD, Medical College of Virginia,1991
Current Research: The general goal of my laboratory is to investigate signal transduction mechanisms for cardiac and smooth muscle cell regulation in order to develop therapeutic strategies against various heart and lung diseases. I have a long-standing interest in how redox processes regulate cell signaling, and my laboratory continues to contribute to the understanding of the mechanism of redox signaling. Another major focus of my laboratory is to study mechanisms of cell growth and death in pulmonary vascular smooth muscle and right heart muscle. We seek to develop therapeutic strategies to treat pulmonary hypertension patients, without adversely affecting the weakened right heart.

Stefano Vicini

Professor, Pharmacology & Physiology
Vicini Lab Website
(202) 687-6441
Office: BSB, 225
Lab: BSB, 228-230
Education: Ph.D., U Torino, Italy, 1979
Current Research: Using transgenic mice with the two major striatal output pathways labeled we are answering a fundamental question: What role tonic and phasic GABA and NMDA conductance plays in striatal disorders? We are studying the functional consequence of the activation of distinct dopamine receptors on NMDA and GABAa receptor subtypes. Our study has great potential to identify novel therapeutic targets for treating disorders associated with striatal dysfunction including Parkinson’s disease, Huntington’s disease, tardive dyskinesia, Tourette’s syndrome and drug addiction.

Tingting Wang

Assistant Professor, Pharmacology & Physiology
Wang Lab Website
(202) 687-1099
Office: SE407 Med/Dent
Lab:  SE407 Med/Dent
Education: Ph.D., Neurobiology, Duke University, 2009
Current Research:  The brain is incredibly complex and malleable in terms of developmental and learning-related plasticity. Homeostatic signaling systems act to stabilize the function of individual nerve cells and neural circuitry, thereby ensuring robust and reproducible brain function and behavior throughout life. My laboratory investigates the molecular mechanisms that underlie the homeostatic control of the nervous system and studies how impaired homeostatic plasticity is involved in neurological, neuropsychiatric and neurodegenerative disorders. We are particularly interested in the intercellular signals that convey information between neurons and glia during homeostatic plasticity. We use an array of cutting-edge electrophysiological, imaging, molecular and genetic tools in Drosophila melanogaster and mice to address:
1. What is the signaling function of glia in synaptic homeostatic plasticity?
2. How does dynamic regulation of extracellular matrix (ECM) and adhesion molecules modulate synaptic transmission?
3. How do genetic mutations and failed homeostasis contribute to neurological and psychiatric diseases, such as epilepsy, autism spectrum disorders and Alzheimer’s Disease?

Anton Wellstein

Professor, Oncology
Dr. Wellstein’s website
(202) 687-3672
Office: E311a Research Building
Education: MD/PhD Gutenberg University, Mainz, Germany 1973/1977; Pharmacology Habilitation (Dr.Sci.) Goethe University, Frankfurt/M Germany 1985
Current Research:  My laboratory studies mechanisms of cancer progression to invasive and metastatic disease utilized by cancer cells. We study tumor-stroma microenvironment to discover driver pathways of cancer cell invasion and metastasis. One focus is on growth factor signaling and includes molecular analyses, signal transduction, mouse models as well as analysis of patient samples from clinical trials.

There are also a number of adjunct faculty at neighboring institutions that serve as co-mentors for student theses and for laboratories available for rotation projects.