Daniel earned his MD/Ph.D. in the Ben-Gurion University physician-scientist training program. His work at the laboratory for human genetics focuses on deciphering genetic mutations and molecular mechanisms of hereditary neurological diseases through studies of unique inbred kindreds and generation of various disease model systems. In his main project, Daniel delineated roles for CDH2-related pathways in the pathophysiology of attention deficit hyperactivity disorder (ADHD). It is the first description of a monogenic, non-syndromic ADHD, from mutation to an animal model. Notably, the CDH2-mutated mice he generated can serve as a model system for developing novel ADHD therapeutics. In another project, he described a neurological syndrome in the medical literature due to a null SEC31A mutation. With a proposed mechanism for activating Endoplasmic Reticulum stress pathways and Drosophila phenocopy, this novel disease is officially denoted as Halperin-Birk syndrome. These and other mutations he discovered through his work are now part of routine prenatal diagnosis and carrier testing in specific populations in Israel.
Hoping to become a clinician-scientist, Daniel’s postdoctoral work at the Icahn School of Medicine at Mount Sinai, New York, is devoted to promoting axon regeneration after spinal cord injury, a scientific frontier and a significant challenge in neuroscience. Specifically, he will explore the function of aryl hydrocarbon receptor (Ahr), a member of the bHLH-PAS transcription factors that acts as an environmental sensor and regulator of neuronal network homeostasis. This novel study promises to advance a fundamental understanding of transcriptional regulation of regenerative gene programs and provides a path for translation, as an expanding list of pharmacological compounds is available for modulation of Ahr activity.