Sarah R Gilman's research while affiliated with Columbia University and other places
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Publications (3)
Autism spectrum disorders (ASDs) are characterized by phenotypic and genetic heterogeneity. Our analysis of functional networks perturbed in ASD suggests that both truncating and nontruncating de novo mutations contribute to autism, with a bias against truncating mutations in early embryonic development. We find that functional mutations are prefer...
Despite the successful identification of several relevant genomic loci, the underlying molecular mechanisms of schizophrenia remain largely unclear. We developed a computational approach (NETBAG+) that allows an integrated analysis of diverse disease-related genetic data using a unified statistical framework. The application of this approach to sch...
Identification of complex molecular networks underlying common human phenotypes is a major challenge of modern genetics. In this study, we develop a method for network-based analysis of genetic associations (NETBAG). We use NETBAG to identify a large biological network of genes affected by rare de novo CNVs in autism. The genes forming the network...
Citations
... The degree of integra on of the frontal cortex within the wider neural system has been implicated across higher-order cogni ve domains (execu ve func on, inhibi on, working memory, planning, and reasoning) and is involved in mul ple, if not all, neurodevelopmental and neuropsychiatric condi ons (4)(5)(6). Consistent with this, previous studies inves ga ng brain spa otemporal gene expression pa erns have reported that the human prefrontal cortex, and the mid-fetal developmental period, are vulnerable points for neurodevelopmental disorders (5)(6)(7)(8)(9). ...
... Impaired adhesion is closely connected to both cell migration and axon guidance, pathways that exhibit abnormalities in genes associated with the risk of SCZ [103][104][105] . Additionally, there is a BD and SCZ-specific association observed in pathways related to the dynamic regulation and restructuring of cytoskeletal actin 106,107 , cytoskeletal proteins 108 , and cellular communication with ECM 109 . ...
... Dysfunctional neuronal mechanisms during late gestation or postnatal stages have been associated with the origin of cortical and neuropsychiatric disorders [24][25][26][27][28][29][30][31] . However, several works suggest disruption of the spatiotemporal identity of the NSCs as earlier fetal risk events [32][33][34][35][36][37][38] . ...
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