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The Simons Foundation Autism Research Initiative (SFARI) is pleased to announce that it has selected six finalists in response to the 2016 Bridge to Independence Award request for applications (RFA).
Grants awarded through the Bridge to Independence Award program are intended to invest in the next generation of top autism investigators by helping early-career scientists transition from mentored training positions to independent research careers. The program is aimed at senior postdoctoral fellows who are currently seeking tenure-track faculty positions. This is the second consecutive year that SFARI has selected finalists as part of this program.
“We hope the unique timing of these career awards will have a long-lasting influence in engaging the best and brightest to focus on autism research,” says Alice Luo Clayton, SFARI senior scientist.
Finalists were selected through a competitive review process. The distinguished scientific review panel included Moses Chao, Ph.D. (professor, New York University School of Medicine), Gerald D. Fischbach, M.D. (distinguished scientist and fellow, Simons Foundation), Zach W. Hall, Ph.D. (former director of the National Institute of Neurological Disorders and Stroke, 1994-1997) and Story Landis, Ph.D. (former director of the National Institute of Neurological Disorders and Stroke, 2003-2014). Members of the panel weighed the quality of the applicant, the scientific merit of their research proposal and their commitment to autism research.
“This is an excellent program that will help launch very promising new investigators interested in autism research. I was very impressed with the quality of the applicants and the promising research that they proposed,” Story Landis says.
With their finalist notification letters in hand, applicants now have the upcoming year to secure a tenure-track faculty position at a U.S. academic institution. Once approved by SFARI, each grantee will receive a commitment of $450,000 over three years through their faculty institution.
The six finalists are:
Current position:
Postdoctoral fellow in the laboratory of Daniel O’Connor, Ph.D. (Johns Hopkins University)
Proposed research project:
Mechanisms of cortical plasticity in autism
SYNGAP1, a candidate autism risk gene, plays a critical role in regulating synaptic plasticity through its ability to suppress extracellular signal-regulated kinase (ERK)-mediated signaling. This project aims to simultaneously monitor ERK signaling and neuronal activity in mice after sensory stimulation and to assess how deficits in SYNGAP1 expression affect these processes. This research will further our understanding of basic interactions between intracellular signaling and cortical plasticity and how these processes are affected in autism.
Current position:
Resident and postdoctoral fellow in the laboratory of Daniel Geschwind, M.D., Ph.D. (University of California, Los Angeles)
Proposed research project:
Integrative characterization of microglial and astrocyte activation in autism
Multiple lines of evidence point to abnormal activation of microglia and astrocytes in autism and related neurodevelopmental disorders. This project aims to use functional genomics, transcriptomics and in vivo human brain imaging to characterize the fundamental properties of glial cell activation in autism and to provide a more complete understanding of the contribution of these cell types in autism pathophysiology.
Current position:
Postdoctoral fellow in the laboratory of Rudolf Jaenisch, Ph.D. (Whitehead Institute for Biomedical Research)
Proposed research project:
Modeling autism using genome engineering in human 2D and 3D neural systems
Hundreds of candidate autism risk genes have been identified to date, although their contributions to the condition remain unclear in most cases. The proposed research project will develop in vitro models of autism by generating isogenic human pluripotent stem cells harboring autism risk gene variants. The stem cell lines will be differentiated into neurons, astrocytes, oligodendrocytes and microglia. Neuron-glia co-cultures in 2D and 3D will be generated and analyzed at different stages of development to reveal cellular phenotypes associated with autism.
Current position:
Postdoctoral scholar in the laboratory of Arnold Kriegstein, Ph.D. (University of California, San Francisco)
Proposed research project:
Cell-type specificity of autism risk factors in the developing human brain
Recent studies have highlighted enriched expression of genes implicated in autism during midfetal stages of human cortical development, but specific developmental events or cell types that may be at risk remain unclear. The current project aims to determine whether the mTOR signaling pathway, which has been linked to autism, regulates the specification of radial glia cells during development. The project will also assess whether radial glia cells orchestrate the development and maturation of resident microglia and if immunological challenges affect this process. Such research will provide new insights into how interactions between autism risk genes and environmental risk factors affect human cortical development.
Current position:
Postdoctoral fellow in the laboratory of Bernardo Sabatini, Ph.D. (Harvard Medical School)
Proposed research project:
Disruption of basal ganglia maturation by cortical hyperactivity in autism
Maturation of basal ganglia striatal circuits in mice is influenced by cortical activity, and aberrant corticostriatal development has been implicated in autism. The proposed research aims to characterize the effect of cortical hyperactivity on striatal structure and function across development. It will also address whether hyperactive corticostriatal circuits during early development contribute to the emergence of repetitive behaviors and motor stereotypies in autism.
Current position:
Research associate in the laboratory of Shai Shaham, Ph.D. (Rockefeller University)
Proposed research project:
Glial control of neuronal shape and function
Glia are increasingly implicated in a number of neurological and neurodevelopmental disorders. However, the molecular mechanisms governing glia-neuron interactions in both healthy and disease states remain poorly understood. This proposal aims to use an established in vivo C. elegans glia-neuron model system to perform detailed analyses of the molecular and cellular mechanisms controlling glia-mediated alterations to neuronal dendritic spines. These studies will help inform our knowledge of how glial dysregulation can contribute to autism etiology.
