Meet Our 2026 Distinguished Investigators
In 2026, the Brain & Behavior Research Foundation awarded Distinguished Investigator Grants valued at $1 million to 10 senior-level scientists who are conducting groundbreaking research in neurobiological and behavioral science. Recipients of the $100,000, one-year grants are exploring critical areas of mental health, including depression, autism spectrum disorder, PTSD, bipolar disorder, schizophrenia, cocaine use disorder, and chronic cannabis use.
Recipients of the Distinguished Investigator Grants are full professors at research institutions in the United States and abroad. They were selected by a committee of the BBRF Scientific Council, which is comprised of 191 experts across disciplines in brain and behavior research who review grant applications and recommend the most promising ideas to fund.
The Recipients of the 2026 Distinguished Investigator Grants are as follows:
Ravi Allada, M.D., University of Michigan, suggests that understanding the biological connection between bipolar disorder, sleep, and circadian rhythms could transform how we diagnose, monitor, and treat this condition. His project seeks to connect risk genes for bipolar disorder to biological mechanisms and clinical outcomes. This could identify new biomarkers for diagnosing and monitoring the illness, such as blood-based tests of circadian rhythm strength. They may also point to new treatment strategies, including optimizing the timing of existing medications or more effective use of circadian-based therapies like light and melatonin.
Paola Arlotta, Ph.D., Harvard University, has used human brain organoids—stem-cell-derived cell-culture models of human brain tissue—to show that when mutated, multiple genes associated with autism spectrum disorder (ASD) risk share an early developmental pattern in which inhibitory neurons develop out of step with the excitatory neurons they wire with. She hypothesizes this type of early asynchronous development of inhibitory neurons leads to later abnormalities in the activity and function of brain circuits, and that this mechanism may be shared across many ASD risk genes. This project seeks to directly test this hypothesis by examining circuit activity in human brain organoids mutant for the ASD risk gene ARID1b.
Christopher W. Cowan, Ph.D., Medical University of South Carolina, is interested in single-gene causes of autism spectrum disorder (ASD) that account for a significant fraction of ASD cases. Mutations or deletions in these single genes are often associated with profound autism and a constellation of commonly co-occurring symptoms that constitute a syndrome. One such gene is MEF2C, which encodes a protein that regulates neurotypical brain development and function. Loss-of-function mutations or deletions in one copy of MEF2C cause a syndrome (MCHS) which is characterized by ASD, language deficits, seizures, intellectual disability, sleep disturbances, immune dysfunction, and motor and sensory system deficits. MEF2C genetic variation is also linked to risk for bipolar disorder, major depressive disorder, and schizophrenia. This project seeks to advance an RNA-based therapeutic approach to treat MCHS.
Aline Desmedt, Ph.D., NeuroCenter Magendie U1215 (INSERM, France), has developed an animal model that reproduces in mice the two memory components of PTSD: traumatic hypermnesia—the intense, involuntary, and recurrent re-experiencing of traumatic memories, often presenting as flashbacks or intrusive thoughts; and contextual amnesia, i.e., remembering details or events but forgetting the surrounding circumstances. This distinguishes PTSD-like memory from normative fear memory. This project seeks to identify neural mechanisms underlying the switch to and from pathological (PTSD-like) to normative fear memories. In animal models, the team will investigate the fate and representation of the “memory engram” during the formation, prevention, and normalization of trauma representation. The aim is to determine the extent to which a memory trace is transformed when (re)contextualized traumatic memory is normalized, shedding light on neurobiological mechanisms that could inform development of new therapeutic and preventive strategies.
Karen D. Ersche, Ph.D., University of Cambridge, UK, seeks to identify underlying mechanisms that drive maladaptive behavior in cocaine use disorder (CUD). One such mechanism may involve endocrine disruption. Cocaine impacts both the hypothalamic–pituitary–adrenal (HPA) and hypothalamic–pituitary–gonadal (HPG) axes, which regulate cortisol and testosterone, respectively, and influence cognition and emotion via various brain networks including the amygdala and orbitofrontal cortex. This project seeks to illuminate the behavioral relevance of hormonal imbalance in chronic cocaine users based on a cohort of 180 adults, investigating endocrine, behavioral, and neural markers of decision-making and emotion processing. It will explore, for example, how neuroendocrine dysfunction relates to risky and social decision-making in CUD. The hope is to uncover new targets for intervention, and ultimately to improve outcomes.
Stephen J. Glatt, Ph.D., The Research Foundation for the State University of New York, Upstate Medical University, is working to develop the ability to non-invasively profile the molecular dynamics of the living human brain. The premise is that measuring changes in the expression of individual genes in discrete brain regions during periods of risk, illness, and recovery from a brain disorder could reveal new causal pathways and targets for treatment. This project will establish, validate, and disseminate a new and improved computational algorithm called the Brain Gene Expression and Network Imputation Engine (BrainGENIE+), which allows the team to register gene-expression levels and patterns in 10 distinct brain regions using just a blood sample. The goal is to uncover molecular states that underpin brain health and disease in individuals actively suffering from neurodevelopmental, neuropsychiatric, or neurodegenerative disorders and establish an atlas of gene-expression features of the living brain in healthy individuals.
Alicia Izquierdo, Ph.D., University of California, Los Angeles, notes that our brains often discern patterns in randomness. Volatility refers to the speed of change in everyday events. “Volatility beliefs,” or expectations of change, have been linked to paranoia in schizophrenia, with the typical observed direction as a heightened expectation of change and enhanced switching behaviors in those experiencing paranoia. Adaptive behavior should take into account both moment-to-moment randomness, (“stochasticity”), as well as the speed of change (“volatility”). Dissociating these factors in the laboratory is computationally and neurobiologically challenging. In this project, she will use a novel behavioral paradigm and modern systems-neuroscience techniques to identify mechanisms underlying this dissociation in thalamo-frontocortical circuits. Testing how these circuits are involved in dissociating volatility from stochasticity, the team hopes to accelerate understanding of neural circuit modulation in psychosis.
Wei Jiang, M.D., Medical University of South Carolina, notes that while acute or infrequent cannabis use may reduce anxiety, chronic and frequent use is associated with heightened anxiety, depression, and suicidality. But causality remains uncertain and likely involves factors beyond direct effects of the drug. Emerging evidence highlights the role of peripheral influences, including the gut–brain and oral–brain axes, in regulating emotion. The team’s past work suggests chronic heavy cannabis use enriches oral Actinomyces microbes, which induce anxiety-like behavior, mitochondrial dysfunction, and impaired inhibitory neurotransmission. This study investigates the mechanisms by which chronic cannabis use drives anxiety through pathogenic oral microbiota and metabolites, and will explore targeted therapeutic approaches.
Loren L. Looger, Ph.D., University of California, San Diego, will explore a novel pharmacological mechanism that may be exploited to ameliorate depression: the upregulation of serotonin synthesis inside of cells. SSRI medicines inhibit the activity of serotonin transporters, thereby lengthening the amount of time over which extracellularly transmitted serotonin molecules can act at receptors outside of the cell. This mechanism ignores the intracellular aspects of serotonin function. Dr. Looger proposes that upregulation of serotonin synthesis would address both pathways: the extracellular pathways addressed by SSRIs and also intracellular pathways. Recent studies of psychedelics and related drugs like MDMA suggest these drugs may help alleviate depression at least in part via an upregulation of serotonin synthesis and transport to critical brain regions. The team will use a high-throughput drug screen to identify modulators of serotonin synthesis. Compounds discovered from this screen may illuminate molecular pathways involved in serotonin synthesis and trafficking and may serve as lead molecules for the development of new medicines.
Jamie L. Maguire, Ph.D., Tufts University. The goal is to further the development of a novel, evidence-based treatment with transdiagnostic potential for psychiatry. The high incidence of treatment resistance in depression (over 30%), Dr. Maguire suggests, is likely due to the fact that the majority of existing medications fall into similar drug classes and do not treat underlying pathophysiological mechanisms. In search of a new, evidence-based target for therapeutic development, this project focuses on impaired neurosteroid synthesis, implicated in numerous psychiatric illnesses. The team has developed a potential treatment which enhances the synthesis of these endogenous compounds with well-established anxiolytic and antidepressant effects. They have already identified small molecules and now will take next steps to develop a novel treatment with transdiagnostic potential for psychiatric illnesses.
