©iStock.com/Nixken
The Simons Foundation Autism Research Initiative (SFARI) is pleased to announce that it has selected six finalists in response to the 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. “By targeting this particularly critical time in one’s career, we hope this funding will have a tangible impact on sustaining scientific excellence in autism research,” says Alice Luo Clayton, SFARI senior scientist.
Finalists were selected through a competitive review process by a distinguished scientific panel. Members of the panel weighed the quality of the applicant, the scientific merit of their research proposal and their commitment to autism research. “As a new grant mechanism, we weren’t quite sure what to expect, but we were tremendously impressed with the quality of applications. These were not easy decisions,” Luo Clayton says.
With their finalist notification letters in hand, applicants now have until December 1, 2016 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 listed below:
Current position:
Postdoctoral fellow in the laboratory of Jessica Cardin, Ph.D. (Yale University)
Proposed research project:
Developmental dysfunction of inhibition in a genetic model of autism
Dysregulation of GABAergic inhibitory function, particularly parvalbumin-expressing (PV) interneurons, has been suggested as a candidate mechanism underlying autism. The goal of this project is to understand more about the contribution of PV interneurons to autism-related circuit and cognitive deficits by studying a novel genetic mouse model of autism in which PV function is selectively manipulated during development.
Current position:
Postdoctoral fellow in the laboratory of Richard Huganir, Ph.D. (Johns Hopkins University School of Medicine)
Proposed research project:
Sleep-dependent synapse remodeling during development and in Rett syndrome
Sleep is an essential process known to promote cognitive functions such as learning and memory. Many neurological disorders, including Rett syndrome, are associated with sleep abnormalities. The proposed project aims to characterize the molecular changes in central nervous system synapses during sleep and to examine sleep-dependent synapse remodeling during development in a mouse model of Rett syndrome.
Current position:
Senior fellow in the laboratory of Richard Palmiter, Ph.D. (University of Washington)
Proposed research project:
Neural correlates of sensory hypersensitivity in autism spectrum disorder
A large majority of individuals with autism experience hypersensitivity to sensory stimuli. However, little is known about how the brain transforms sensory information into aversive signals. The proposed research aims to identify neural circuits and their corresponding neural structures in the brain stem that are critical for encoding aversive sensory signals. Subsequent experiments will address whether neurons in these circuits are more sensitive to sensory stimuli in autism mouse models compared with wildtype mice.
Current position:
Instructor in neurosurgery in the laboratory of Ziv Williams, M.D. (Massachusetts General Hospital, Harvard Medical School)
Proposed research project:
Neuronal underpinnings of social interactive behavior and its disruption
Deficits in social behavior are among the most prominent and persistent features of autism. The aim of this project is to systematically investigate the single-neuronal, population and causal underpinnings of basic interactive social behavior in a primate model. Such research will provide new insight into how fundamental social computations are performed and modulated at the neuronal level.
Current position:
Senior fellow in the laboratory of Evan Eichler, Ph.D. (University of Washington)
Proposed research project:
In vitro modeling of genetic subtypes of autism
This project aims to use genome engineering technology (CRISPR/CAS9) to create human cell line models of specific de novo mutations in genes that have been proposed as putative ‘genetic subtypes’ of autism due to their strongly associated clinical phenotypes. The primary goal of the research is to understand what effect these mutations have on neural biology and therefore disease etiology.
Current position:
Postdoctoral fellow in the laboratory of Mark Zylka, Ph.D. (University of North Carolina at Chapel Hill)
Proposed research project:
Inhibitory circuit dysfunction in autism spectrum disorder
Duplication or triplication of UBE3A is known to be linked to autism. Moreover, an autism-linked missense mutation in UBE3A has recently been found to result in excessive UBE3A activity and synaptic dysfunction. This research project aims to generate and characterize a mouse model of autism that incorporates this disease-linked mutation. Subsequent experiments will focus on investigating how changes in synaptogenic programs alter patterns of interneuron migration and the functional and behavioral consequences of aberrant interneuron development in this mouse model.
