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Dr. Gruen’s primary research interest involves finding and characterizing genes that cause reading disability, commonly known as dyslexia. Dyslexia is present in 10 to 20% of school children and is the most common cause of learning disability. It is also mostly genetic in origin with genetic factors accounting for 40% to 60% of the poor performance in reading tests. Through genetic studies of families and children with dyslexia, his group identified a major contributing gene, doublecortin-domain-containing-2 (DCDC2) (Meng et al, PNAS 102: 17053-17058, 2005). Moreover, he showed that a deletion in a putative regulatory sequence in DCDC2 is present in ~20% of dyslexics. He has now found 20 variations (alleles) of this regulatory (enhancer) sequence and is working on identifying which alleles are the most deleterious and which may be protective, and how these variations functionally alter brain development using immunocytochemistry, RNAi, a mouse knockout model, and other molecular approaches in animals. His group is also exploring how variations of DCDC2 and other dyslexia genes alter brain activation patterns in human subjects using functional magnetic resonance imaging (fMRI), and brain cytoarchitecture using voxel-based morphometry analyses of gray matter and fractional anisotropy.
A neonatologist by training, Dr. Gruen also studies genetic contributions to common disorders encountered in prematurely born infants. Using heritability analyses of identical and non-identical twins born less than 32 weeks gestational age, he and collaborators found that genetic factors account for at least 45% of the variance in liability for bronchopulmondary dysplasia, a common pediatric form of chronic lung disease (Bhandari et al, Pediatrics, 117(6):1901-1906, 2006), 70% of the variance for retinopathy of prematurity (Bizzarro et al, Pediatrics, 118(5):1858-1863, 2006), and 70% of the variance for the most common congenital heart disease, patent ductus arteriosus (PDA).