Michael Boland is a cellular/molecular biologist with expertise in human stem cell technology, transcriptomics, epigenetics, developmental neurobiology, gene-targeted therapy development, and drug screens. Currently he is the Strategic Director for Translational and Clinical Research at the Center for Epilepsy and Neurodevelopmental Disorders (ENDD) at the University of Pennsylvania's Perelman School of Medicine and the Children’s Hospital of Philadelphia. ENDD is focused on gene-targeted therapy development, multisite natural history studies, and clinical outcomes for STXBP1 and SYNGAP1 disorders.
Prior to joining ENDD, Dr. Boland was an Assistant Professor in the Department of Neurology and the Institute for Genomic Medicine at Columbia University Medical Center (New York, NY). His group took an integrated developmental and functional approach to study genes associated with pediatric epileptic encephalopathy and autism spectrum disorder using patient-derived or genetically engineered human stem cells and genetic mouse models. His group developed cortical organoid models of cortical malformations of development attributed to MAP1B and FLNA mutations, as well as studied neurodevelopmental disorders that result from mutations in GRIN2A, KCNT1, GNB1, and HNRNPU, and disorders of glycosylation/deglycosylation (PMM2, DPAGT1, NGLY1, and SLC35A2). His research focus shifted to the development of gene-targeted therapies for STXBP1 encephalopathy when his infant son was diagnosed with a pathological variant in STXPB1.
Boland obtained his PhD in Biochemistry and Molecular Biology from the University of Nebraska Medical Center (Omaha, NE) where he discovered a new link between epigenetics and DNA repair in embryonic stem cells. He performed his postdoctoral studies at The Scripps Research Institute (La Jolla, CA), where he studied the developmental potential and genomic structural variation of mouse induced pluripotent stem cells via mouse cloning and whole genome sequencing, respectively. He also studied the integration of gene expression and epigenetic abnormalities during early neurodevelopment in a human pluripotent stem cell model of Fragile X Syndrome.