- Rita Allen Foundation

All Scholars

Since 1976, the Rita Allen Foundation has awarded millions of dollars in grants to early-career biomedical scholars. These grants allow Rita Allen Foundation Scholars to establish labs and pursue research directions with above-average risk and promise. See below for a full list of Scholars, or read more about the Rita Allen Foundation Scholars program.

2014

Lei Ding +
Columbia University

Lei Ding

Lei Ding completed his undergraduate studies at Peking University, and earned a Ph.D. at the University of Colorado, Boulder, where he worked with Min Han. He was a postdoctoral fellow in Sean Morrison’s laboratory at the University of Michigan and The University of Texas Southwestern Medical Center. He joined the faculty of Columbia University in 2013.

A lifelong supply of blood and immune cells depends on self-renewing hematopoietic stem cells (HSCs). How HSCs self-renew is a fundamental question with broad implications for understanding development, regeneration, cancer and aging of the blood system. HSC self-renewal is regulated by cell-intrinsic and -extrinsic mechanisms. The Ding laboratory is interested in these mechanisms, particularly extrinsic mechanisms that regulate blood-forming HSC self-renewal and maintenance. Prior work has identified bone marrow perivascular mesenchymal stromal cells as a critical component of the niche.

Ding’s group is studying the extrinsic regulation of HSCs in three distinct, yet closely related, areas: 1) regulation of bone marrow perivascular mesenchymal stromal cells; 2) the cellular component of the fetal liver HSC niche; and 3) the contribution of the niche to the pathogenesis of hematological diseases. They are in the process of characterizing several candidate factors that may regulate the fate of bone marrow perivascular stromal cells. They are also elucidating the roles of several candidate niche cell types in fetal livers. In addition, their data suggest that bone marrow mesenchymal stromal cells are critical contributors to a hematopoietic malignancy, myelofibrosis, providing a cellular target to better treat the disease. HSC-based bone marrow transplantation is widely used in clinics to treat hematological diseases. Ding and his team hope to apply their knowledge to better harness the power of HSCs.
Molly Hammell +
Cold Spring Harbor Laboratory

Molly Hammell

Molly Hammell (Milton E. Cassel Scholar) holds a B.S. in physics from the College of William and Mary and a Ph.D. in physics and astronomy from Dartmouth College. The Hammell lab specializes in developing novel computational algorithms for the analysis and integration of high-throughput genomics datasets and applying these to questions of human disease. Hammell has a broad background in small RNA biology and gene regulatory network analysis, transposon biology and genomics, as well as extensive experience in the statistical analysis of next-generation sequencing data. As a postdoctoral fellow working with Victor Ambros at Dartmouth Medical School and the University of Massachusetts Medical School, she developed new algorithms to identify the targets and pathways regulated by microRNAs in animals and to profile the dynamics of small RNA activity across development. Her lab at Cold Spring Harbor Laboratory has expanded on these efforts to map the role of both microRNAs and transposon-targeting piRNAs and siRNAs in animals. This includes efforts to establish the molecular mechanisms by which transposons are controlled in somatic tissues. This also includes a major project to profile the genomes and transcriptomes of amyotrophic lateral sclerosis (ALS) patient samples in order to understand the extent to which transposons contribute to neurodegenerative disease in patients.

Our genomes are filled with viral-like sequences called transposons, many of which are capable of creating new copies of themselves that can reintegrate elsewhere in the genome, altering the function of nearby genes. While most transposon sequences are now-defunct remnants of ancient genomic parasites, a small fraction of these are still capable of activating themselves, creating genomic instability and crippling cellular function. The Hammell lab and others have discovered a link between the activity of these transposon sequences and neurodegenerative diseases related to misfunction of the RNA binding protein TDP-43 (ALS and frontotemporal lobar degeneration). However, much remains unknown about how transposons are controlled in somatic tissues such as the brain, and the extent to which their activity contributes to neurodegenerative disease. Hammell’s group is working to elucidate the connections between transposon activity and TDP-43 related diseases.
Sebastian Klinge
The Rockefeller University
Zachary Knight
University of California, San Francisco
Gregory Scherrer +
University of North Carolina at Chapel Hill School of Medicine (Stanford University School of Medicine)

Gregory Scherrer

Gregory Scherrer (Award in Pain Recipient) earned his Ph.D. in cellular and molecular biology from the University of Strasbourg, France. He completed postdoctoral training at the University of California, San Francisco, and at Columbia University. He joined the faculty at the Stanford University School of Medicine in 2012. In addition to a Rita Allen Foundation Scholar award, he has received an International Association for the Study of Pain Postdoctoral Fellowship, National Institutes of Health/National Institute on Drug Abuse K99R00 Pathway to Independence and R01 Awards, a Department of Defense Neurosensory Research Award, and an International Narcotics Research Conference Young Investigator Award, and most recently was named a New York Stem Cell Foundation – Robertson Neuroscience Investigator.

The members of the Scherrer Laboratory investigate how the nervous system generates the sensory and affective dimensions of pain experience and opioid analgesia to discover novel analgesic therapies. They aim to identify the pathological changes that occur within neural circuits when chronic pain develops, at the neural network, cellular and molecular levels. One of their approaches is to gain understanding of how our endogenous opioid system modulates pain thresholds. Opioid receptors mediate the effects of opioid painkillers, such as morphine. By determining how opioids generate analgesia and detrimental side effects (e.g., tolerance, addiction, respiratory depression), Scherrer and his team hope to develop more efficient and safer analgesics for the treatment of chronic pain. These studies will also identify novel approaches to counteract opioid side effects and battle the current opioid epidemic. To reach these goals, Scherrer’s research combines a variety of experimental approaches, including molecular and cellular biology, neuroanatomy, electrophysiology, opto- and pharmacogenetics, in vivo calcium imaging and behavior.
Lin Tian +
University of California, Davis, School of Medicine

Lin Tian

Lin Tian holds a B.S. in neuroscience from the University of Science and Technology of
China and a Ph.D. in biochemistry, molecular and cell biology from Northwestern University. She completed postdoctoral training at the Howard Hughes Medical Institute’s Janelia Farm Research Campus, where she developed a toolbox of ultrasensitive neural activity sensors that have been widely utilized. Her current work is a combination of neural activity sensor development and applications. Tian has received the National Institutes of Health Director’s New Innovator Award, Human Frontier Science Program Young Investigator Grant, Hartwell Foundation Individual Biomedical Research Award and NIH BRAIN Initiative grants.

The altered dynamics of synaptic transmission have been implicated in a number of human neurological and psychiatric diseases, including Parkinson’s, schizophrenia and addiction. However, how complex patterns of neural activity at multiple synapses interact to drive changes in circuit connectivity remains poorly defined. To address this question, we must determine the spatiotemporal relationships of different types of neurotransmitters and neuromodulators with synaptic resolution in a defined circuitry. Recent breakthroughs in modern microscopy and protein-based fluorescence sensors hold great promise to access synaptic transmission with needed molecular and cell type specificity and spatiotemporal resolutions. Tian and her collaborators have generated a sensor for the excitatory neurotransmitter glutamate and demonstrated its utility for detection of fast signaling events in worm, fish, fly and mouse. To further expand the kinds of neural activity that can be measured with genetically encoded indicators, they applied the established sensor design and optimization platform to the development of a set of specific, targetable and sensitive sensors for direct measurement of neurotransmitters, including gamma-aminobutyric acid and the biogenic amines. Application of these imaging tools will enable neuroscientists to obtain a dynamic and comprehensive view of synaptic transmission in action to decipher the codes for transferring information across neural circuitry and systems.
Tuan Trang +
University of Calgary

Tuan Trang

RELATED STORY: Rita Allen Foundation Scholars Reveal Biological Forces That Underlie Responses to Change

Tuan Trang (Award in Pain Recipient) began his research career as an undergraduate at Queen’s University studying the effects of prenatal alcohol exposure. He also completed a Ph.D. in pharmacology and toxicology there, researching the spinal mechanisms of opioid analgesia with the goal of developing new pharmacological strategies for improving pain therapy. He pursued postdoctoral training as a Canadian Institutes of Health Research (CIHR) fellow in the laboratory of Dr. Michael Salter at the Hospital for Sick Children in Toronto. He has received a CIHR New Investigator Award, and young investigator awards from the Canadian Association for Neuroscience and Canadian Society for Pharmacology and Therapeutics. His research has been supported by grants from, in addition to the Rita Allen Foundation, the CIHR, the Natural Sciences and Engineering Research Council of Canada, a Vi Riddell Pain Grant from the University of Calgary and the Canada Foundation for Innovation.

Opioids are among the most powerful and widely prescribed drugs for treating pain. However, a major problem in terminating opioid pain therapy is the debilitating withdrawal syndrome that can plague chronic opioid users. The mechanisms involved in opioid withdrawal are poorly understood, and the limited clinical strategies for treating withdrawal are ineffective. Trang and his collaborators have identified the pannexin-1 (Panx1) channel as a novel therapeutic target for treating morphine withdrawal. They discovered that morphine treatment induces synaptic plasticity in spinal lamina I/II neurons, which manifests as long-term synaptic facilitation upon naloxone-precipitated morphine withdrawal. This synaptic facilitation is critically gated by activation of Panx1 channels expressed on microglia. Pharmacologically blocking Panx1, or genetically ablating this channel specifically from microglia, blocked spinal synaptic facilitation and alleviated the behavioral sequelae of morphine withdrawal. Their findings together reveal a novel mechanism by which microglia signal through Panx1 to produce the cellular and behavioral corollary of withdrawal. Thus, targeting Panx1 represents a potential novel therapeutic approach for treating the symptoms of opioid withdrawal. Trang and his team are moving these discoveries into the clinic by building on the utility of probenecid as a unique and practical therapy for the management of opioid withdrawal. In a pilot clinical trial, they will test whether probenecid alleviates opioid withdrawal in patients undergoing opioid tapering, a systematic and gradual approach intended to reduce or discontinue opioid use.

Skip to content Rita Allen Foundation Years 2014

All Scholars

See Scholars by Name/Year