Faculty available for committees

AZA Allsop is an artist, neuroscientist, and psychiatrist who conducts research at the intersection of social cognition, music mindfulness, and psychedelics. His research and clinical work is guided by the belief that decoding these tools will provide a better understanding of how social groups function and offer insights into treating mental suffering and enhancing the evolution of society at large. AZA studied Biology, Philosophy, and Jazz Studies at North Carolina Central University, received his MD from Harvard Medical School, PhD in Neuroscience from MIT and was an Emerson Scholar at Berklee College of Music. He completed his residency in the Department of Psychiatry at Yale University where he served as co-chief resident of the Clinical Neuroscience Research Unit and completed a certification in psychedelic therapy and research. He is currently an Assistant Professor in Yale’s Department of Psychiatry and Director of the Center for Collective Healing at Howard University. He teaches meditation, yoga, and music and has co-founded several companies that combine arts, science, and community building to drive social change.

Dr. Cortes-Briones is an Assistant Professor in the Department of Psychiatry at Yale University, Technical Director of MEG Imaging for Neuropsychiatric Disorders (MIND) Center at the West Haven VA Healthcare System, and a member of the Schizophrenia Neuropharmacology Research Group at Yale (SNRGY) as well as the Yale Center for the Science of Cannabis and Cannabinoids (YC-SCAN2). His primary research interests include understanding the changes in brain dynamics underlying the acute effects of psychoactive substances such as tetrahydrocannabinol (THC) and ketamine, as well as auditory verbal hallucinations in individuals with schizophrenia. His current work focuses on applying machine learning algorithms to transcribe inner speech and auditory verbal hallucinations from their electrophysiological correlates, reconstructing fetal electroencephalographic (EEG) data from signals collected noninvasively from the maternal abdomen, and using magnetoencephalography (MEG) to study the acute effects of THC on information transmission, modification, and storage in the human brain, as well as the changes in excitatory-to-inhibitory balance in schizophrenia and other psychiatric disorders.

Dr. Charles A. Greer is the Vice Chair for Research and holds the rank of Professor of Neuroscience. Dr. Greer also serves as Director of the Yale Interdepartmental Neuroscience Graduate Program. He has served as the President of the Association for Chemoreception Sciences, Chair of National Institutes of Health Study Sections and recently completed a term on the Advisory Council for the National Institute of Deafness and Other Communicative Disorders. He has organized several national and international conferences and is frequently an invited speaker. Dr. Greer is an Associate Editor of The Journal of Comparative Neurology and Journal of Neuroscience and a member of the editorial boards of Frontiers in Neurogenomics, Frontiers in Neuroanatomy and Frontiers in Neuorgenesis and the Faculty of 1000. Dr. Greer has been the recipient of numerous awards recognizing his research accomplishments.

Horwich received undergraduate and M.D. degrees from Brown University, trained in Pediatrics at Yale, was then a postdoctoral fellow first at Salk Institute in the Tumor Virology Laboratory, and then in Genetics at Yale, then joined the Yale faculty. His work was initially involved with protein import into mitochondria and resulted in discovery of a "folding machine" inside mitochondria, Hsp60. He has used genetic, biochemical, and biophysical tools to study the mechanism of action of these ring shaped so-called chaperonin machines that provide essential assistance to protein folding in many cellular compartments. More recently he has focused on neurodegenerative disease, modeling mutant SOD1-linked ALS in mice transgenic for a mutant SOD1 fused with a YFP reporter. In the transgenic mutant strain, the mutant SOD1 misfolds and lodges the fusion protein in YFP fluorescent aggregates, visible in motor neurons by 2-3 months of age. These neurons are removed by microglial cells, associated with loss of ~50% of motor neurons. By 6-7 months of age the mice exhibit lower extremity paralysis, associated with loss of ~50% of the remaining motor neurons. By contrast, a wtSOD1-YFP transgenic strain with the same amount of total SOD1-YFP protein in spinal cord remains asymptomatic even after two years, and the spinal cord remains free of aggregates. An early study showed that overexpression of the molecular chaperone Hsp110, known to be part of a chaperone disaggregase, improved survival of the SOD1-YFP mice. Additional genetic modifiers are being tested.

I am a board certified psychiatrist and neuropsychiatrist with research work that has been translational in nature and focused on elucidating the underlying pathology of brain conditions such as Autism Spectrum Disorder, substance abuse and neuropsychiatric disorders (e.g., Parkinson's disease) with an aim to find effective clinical treatments guided by molecular neuroimaging. Studies have included using in vivo PET imaging to investigate the role of neuroreceptors such as dopamine D3, serotonin 1B and 6, MGlur5 and kappa opioid systems, neuroinflammation, and most recently, synaptic density (SV2A) in clinical and nonclinical populations. Ongoing interests include imaging neuropsychiatric and addictive disorders and the demographic, social and environmental factors influencing our brain.

Angus Nairn did his undergraduate training in biochemistry at the University of Edinburgh, Scotland and his PhD in muscle biochemistry in the laboratory of Professor Sam Perry at Birmingham University, England. He then carried out postdoctoral research in molecular neuroscience with Professor Paul Greengard at Yale, and moved with Professor Greengard to Rockefeller University in 1983 as a faculty member. He moved back to Yale University in 2001, where he is currently the Charles B.G. Murphy Professor of Psychiatry. He also holds a joint appointment in the Department of Pharmacology and is co-director of the Yale/National Institute of Drug Abuse Neuroproteomics Center at the Yale School of Medicine.

Michael Nitabach JD, PhD is faculty member of Molecular Cell Biology, Genetics and Development, Molecular Medicine, Pharmacology and Physiology, and Interdepartmental Neuroscience Program. He is affiliated with the Program in Cellular Neuroscience, Neurodegeneration and Repair. He received a PhD from Columbia University and a JD from New York University.

Dr. Pasquini graduated in Medicine at the University of Florence in 2014, completed a Radiology Residency and a PhD in Neuroplasticity at La Sapienza University in Rome in 2019 and 2023 respectively, with a PhD thesis defense on language reorganization in the preoperative planning of brain tumors. In Italy, Dr. Pasquini served as Neuroradiology faculty at La Sapienza University and Bambino Gesù Children’s Hospital in Rome. In the US, Dr. Pasquini served as Research Associate in the fMRI laboratory at Memorial Sloan Kettering Cancer Center, completed one year of Clinical Fellowship in Neuro-Oncology Imaging and a Nuclear Medicine Residency at Memorial Sloan Kettering Cancer Center between 2020 and 2024. Dr. Pasquini published >45 papers in peer reviewed journals. His contribution to the understanding of brain plasticity has been recognized internationally with multiple awards from the major US and international radiological societies, including the RSNA Research Trainee Award in 2018, RSNA Fellow Grant in 2021, ASNR Research Fellow Award in 2022, ARRS Resident Executive Council Award in 2023, ACNM Resident Research Award in 2024.

Professor Rudnick is a graduate of Antioch College, where he received a B.S. in Chemistry in 1968. He performed graduate studies in the enzymology of amino acid racemases in the laboratory of Robert H. Abeles in the Graduate Department of Biochemistry at Brandeis University, receiving a Ph.D. in Biochemistry in 1974. His graduate studies led to an understanding of the structure and mechanism of proline racemase that was confirmed by the crystal structure of a homologous protein in 2006. From 1973-1975, Professor Rudnick performed postdoctoral research on lactose permease with H. Ronald Kaback at the Roche Institute of Molecular Biology. This work provided a greater understanding of binding and transport reactions using photoaffinity reagents and substrate analogs. In 1975, he left Roche to become an Assistant Professor in the Department of Pharmacology at Yale, and was promoted to Associate Professor in 1980 and Professor in 1991. Professor Rudnick’s research at Yale has focused on the mechanism and structure of mammalian serotonin transporter (SERT). He developed a system of platelet plasma membrane vesicles with which to study the bioenergetics and mechanism of transport. These studies provided an understanding of the coupling of ion gradients to serotonin accumulation and also identified SERT as the molecular target for the antidepressant imipramine and the psychostimulant MDMA (ecstasy). Beginning in the 1990s, Professor Rudnick’s laboratory has been studying the molecular characteristics of SERT and other neurotransmitter transporters expressed in cultured cells. These studies led to the identification of the serotonin binding site in SERT and of regions in the protein undergoing conformational changes during transport. The availability of a crystal structure for a homologous bacterial transporter in 2005 allowed Professor Rudnick and his colleagues to use the conformational changes to propose a conformational mechanism of transport that is gaining wide acceptance. Because SERT is structurally related to many other transporters, the proposed mechanism is likely to apply to transporters functioning in many diverse biological systems. In addition to these mechanistic studies, Professor Rudnick’s laboratory has been investigating a spontaneously occurring SERT mutant associated with several psychiatric disorders. The mutation apparently inhibits removal of a phosphate group added to SERT by cGMP-dependent protein kinase. The mechanism by which this phosphate increases SERT activity is an active area of investigation.