The Nancy Lurie Marks Family Foundation Postdoctoral Fellows Fund at Harvard Medical School

Under the direction of David E. Golan, MD, PhD, the Dean for Research Initiatives and Global Programs, the primary focus of the Nancy Lurie Marks (NLM) Family Foundation Postdoctoral Fellows Fund is to provide support for the following five postdoctoral fellows focused on autism research at Harvard Medical School for two-year terms.

Elizabeth Lackey, PhD (Regehr Lab)
“Circuit specializations of cerebellar regions that regulate social behaviors”

Elizabeth’s research reveals that the cerebellum—a brain region traditionally linked to movement and balance—plays a crucial role in social behaviors that are disrupted in autism spectrum disorder (ASD). Using mouse models, she discovered that when specific cells called Purkinje cells malfunction in particular areas of the cerebellum (Crus I and II regions), mice develop severe social difficulties while their movement remains normal. Her current work examines how different brain circuits within the cerebellum process information and contribute to various social behaviors. This groundbreaking research suggests that targeting cerebellar dysfunction could offer new therapeutic approaches for treating social challenges in ASD.

Alex Wang, PhD (Fishell Lab)
“How SCN2A Mutations Disrupt Brain Communication in Autism”

Alex investigates how mutations in SCN2A, one of the most important autism risk genes, disrupt brain function and lead to autism-like behaviors. This gene controls sodium channels that help brain cells communicate. When SCN2A is faulty, it reduces the activity of excitatory neurons in the brain’s frontal cortex—an area crucial for social behavior and flexible thinking. Alex’s research focuses on how these changes affect inhibitory neurons, which act like brakes in brain circuits. Using advanced imaging and computer modeling, he aims to understand how disrupted communication between different types of brain cells contributes to autism symptoms, potentially leading to targeted treatments.

Bruno Gegenhuber, PhD (Greenberg Lab)
“Glucocorticoid receptor signaling promotes astrocyte maturation to restrict cortical plasticity”

Bruno studies “critical periods”— special windows during early brain development when experiences shape how neural circuits form. His research discovered that corticosterone, a stress hormone, works with brain support cells called astrocytes to close these critical periods. This timing mechanism is often disrupted in autism, leading to abnormal sensory processing. Bruno found that corticosterone levels naturally rise when young animals first open their eyes, and this surge helps mature the brain’s response to sensory input. Understanding how this hormone-astrocyte pathway controls brain plasticity could lead to treatments that restore proper critical period timing in autism spectrum disorders.

Tomasz Kula, PhD (Sabatini Lab)
“High throughput screening of genetic risk factors in the adult mouse brain”

Tomasz developed revolutionary technology to study how multiple autism-related genes contribute to the disorder simultaneously. Since autism involves hundreds of different genetic mutations, studying each one individually in animal models is extremely time-consuming and expensive. His innovative approach allows researchers to introduce different genetic mutations into individual brain cells within the same animal, creating a “genetic mosaic” brain where each cell carries a different autism-associated mutation. This breakthrough enables scientists to compare how various genetic changes affect different types of brain cells at once, potentially revealing common patterns underlying autism symptoms despite diverse genetic causes.

Guangqing Lu, PhD (Huh Lab)
“Mapping IL-17’s Therapeutic Pathways in the Brain”

Guangqing’s research focuses on interleukin-17 (IL-17), an immune system molecule that surprisingly shows promise for treating autism symptoms. His lab discovered that IL-17 receptors in the brain, when activated, can temporarily improve social behavior and reduce repetitive behaviors in mouse models of autism—regardless of the underlying genetic cause. To understand how this works, Guangqing developed an innovative tracking system called CyCLoPs that uses fluorescent signals to identify exactly which brain cells respond to IL-17 treatment. This technology allows researchers to map the specific brain regions and cell types involved in IL-17’s therapeutic effects, potentially leading to new immunotherapy-based treatments for autism and other neurodevelopmental disorders.