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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.

2025

Alexander Chamessian +
Washington University School of Medicine in St. Louis

Alexander Chamessian

Assistant Professor, Anesthesiology

B.Sc., Stony Brook University

M.D., Ph.D., Duke University School of Medicine

Chronic pain affects more than 50 million Americans, and current treatments often rely on opioids, which can be addictive and ineffective for many people. The Chamessian Lab is exploring a promising new way to relieve pain using an emerging therapeutic modality called targeted protein degradation (TPD), which eliminates protein targets rather than just blocking them. This project will apply TPD to the voltage-gated sodium channels NaV1.7 and NaV1.8, both of which are key mediators of pain in humans. The proposed work builds on foundational in vitro results from the Chamessian Lab showing for the first time that NaV1.7/8 are amenable to TPD using small molecule effectors called PROTACs. Now, Alexander Chamessian and his team will 1) test the ability of PROTAC-mediated TPD of NaV1.7/8 to produce analgesia in vivo using preclinical animal models, and 2) develop new tools to more selectively direct TPD to pain-generating neurons (nociceptors). Taken together, this work is poised to deliver novel, non-addictive degrader analgesics to bring much needed relief to the millions of people suffering from chronic pain.
Lamia Wahba +
The Rockefeller University

Lamia Wahba

Assistant Professor, Genetics and Genomics

B.Sc., College of William and Mary

Ph.D., Johns Hopkins University

In the last months of 1944, towns in Western Netherlands plunged into the Hongerwinter, a six-month period of acute famine brought on by World War II. Nearly six decades later, a landmark study revealed that descendants of the Dutch survivors suffered adverse health effects two generations down. How did hunger impact their grandchildren’s lifespan?

External factors such as diet and stress have been linked to adverse consequences transmissible to offspring. This notion that environmentally-induced changes in an organism’s physiology can be passed on to offspring—once dismissed as heresy—has now gained widespread acceptance. However, critical questions on the prevalence and stability of such induced traits remain. Whether mechanisms driving these seemingly non-genetic changes could enable more rapid evolution in response to new environments than genetic alterations alone remains unclear. Addressing these questions drives research in the Wahba Lab, where Lamia Wahba and her team seek to answer a fundamental question facing biologists today: Do we need to radically rethink our views on inheritance to account for nongenetic mechanisms?
Deepshika Ramanan +
Salk Institute for Biological Studies

Deepshika Ramanan

Assistant Professor, Molecular Biology

B.Sc., Winona State University

Ph.D., New York University

Maternal protection of offspring through milk is fundamental across mammals, yet the underlying immune mechanisms remain poorly understood. Breastmilk contains immune factors such as antibodies that not only defend against pathogens but also shape the infant’s gut immunity and influence lifelong health. However, what determines the immune composition of breastmilk and how it impacts infant intestinal immunity is still unclear. The Ramanan Lab studies the entero-mammary axis—the bidirectional communication between the gut and mammary gland—to understand how maternal immunity is transferred through milk. Using multi-omic approaches, the lab aims to uncover how immune cells and other signals from the gut influence maternal mammary gland and milk composition, and how these components protect the offspring from infections and autoimmune diseases.
Christopher Lapointe +
Fred Hutchinson Cancer Center

Christopher Lapointe

Assistant Professor, Basic Sciences Division

B.A., Colby College

Ph.D., University of Wisconsin-Madison

Cells contain tens of millions of protein molecules responsible for conducting the many functions required for life, including sending nerve signals, tightening muscles, fighting off viruses and more. These proteins are made by tiny molecular machines called ribosomes, which use the information stored in genes to build the proteins found in cells. At any given moment, millions of ribosomes must find the correct set of genetic instructions and start reading them at exactly the right spot. When this critical process goes awry, it can lead to many diseases, including cancer, developmental disorders, autoimmune diseases, and neurodegenerative conditions.

The Lapointe Lab uses cutting-edge technologies that capture ‘molecular movies’ of individual ribosomes at work, to see and understand how healthy cells control protein production and how this control breaks down in disease. These discoveries will help reveal potential new strategies for treating disorders connected to ribosomal dysfunction.
Martin Taylor +
Brown University

Martin Taylor

Assistant Professor, Pathology and Laboratory Medicine

Milton E. Cassel Scholar

B.S.E., Princeton University

M.D., Ph.D., Johns Hopkins University School of Medicine

Genes make up only 2 percent of the human genome. In contrast, half the genome is around two million copies of the same few transposon sequences, which for years were relegated as “junk DNA.” Transposons are virus-like, self-copying DNA parasites. In humans, there is one class of active transposon, called LINE-1. Among hundreds of thousands of inactive copies and fragments, humans inherit 150–200 active copies of LINE-1, which are repressed in healthy tissues by multiple redundant mechanisms. In cancer, autoimmunity, and diseases of aging such as Alzheimer’s, LINE-1 escapes repression and contributes to disease pathology by mutating the genome and causing inflammation. The goals of the Taylor Lab are to 1) understand how LINE-1 works in detail and how much of a contribution it makes in these diseases, 2) develop new strategies to target LINE-1 for prevention and therapy, and 3) develop new diagnostics to find disease earlier, where interventions are most effective.
Allan-Hermann Pool +
UT Southwestern Medical Center

Allan-Hermann Pool

Assistant Professor, Neuroscience, Anesthesiology and Pain Management

B.Sc., Tallinn University of Technology

Ph.D., University of California, Berkeley

Animals have evolved the ability to discriminate between different types of tissue injuries and perceive them as distinct pain states. The Pool Lab seeks to understand cellular mechanisms through which the spinal cord translates tissue damage into central pain perception and orchestrates adaptive and maladaptive pain behaviors. To this end, the Pool Lab is studying the functional role of diverse spinal cord output neuron classes that link the spinal cord to the central brain and give rise to all pain perception below the neck. Furthermore, the lab aims to develop a new therapeutic avenue to selectively mute pain-conveying spinal cell types based on cellular features that differentiate them from the rest of the delicate spinal cord circuitry. Consequently, Allan-Hermann Pool and his team hope to identify new cellular and molecular targets for precision control of the perception of pain.
Alex Johnson +
Brandeis University

Alex Johnson

Assistant Professor, Biochemistry

B.A., Reed College

Ph.D., Stanford University

All cellular life is defined by membranes. At the edge of the cell, the plasma membrane forms a barrier against external insults, and internally, organellar membranes compartmentalize crucial cellular processes. Proteins embedded within membranes allow for the regulated passage of biomolecules and communication within and between cells. As a result, membranes are a focal point of immune signaling pathways and a chief target of pathogens that seek to destroy cells. Alex Johnson discovered that an immune signaling mechanism used by human cells is billions of years older than expected and deployed by bacteria to defend against their major pathogens, bacteriophages. In cells, this mechanism relies on an incredible class of proteins that form gigantic pores in membranes, effectively “poking holes” that induce cell death and the secretion of immune signaling molecules. By studying bacterial homologs of these pore-forming proteins, Johnson’s work established a new frame of reference to understand how these proteins work and yielded unforeseen insights into their mechanism of regulation in human cells. The broad goal of his lab’s research program is to answer stubborn problems of immunology using a comparative evolutionary analysis. Currently, the lab of Microbes and Biochemistry at Brandeis University is focused on applying a pan-species analysis to reveal the full breadth of mechanisms used by pore-forming proteins and applying this knowledge to develop pore-forming proteins as a new therapeutic modality.

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