On January 26, 2018, SFARI held a workshop to discuss the use of zebrafish in autism research. Experts in both rodent and fish models discussed key issues in the field, including zebrafish mutant construct validity, the visualization of circuit development and function, and high-throughput phenotyping and pharmacological screens for translational opportunities.
SFARI held its fourteenth science meeting September 30–October 2, 2018. SFARI investigators, collaborators and foundation staff came together to discuss recent findings in autism genetics, molecular and system-level mechanisms, as well as clinical studies. The meeting featured keynote and session presentations, in addition to demo sessions of online platforms for visualizing and analyzing data sets relevant for autism research.
Findings from the first SPARK genetics study have now been published. The study, which analyzed whole-exome and genome-wide genotyping data from 457 autism families, confirmed known genetic findings and identified new candidate autism risk genes.
Lilia Iakoucheva and colleagues found that mice lacking a copy of the high-confidence ASD risk gene Cul3 have reduced brain volumes, potentially due to defects in Rho signaling during brain development.
SFARI is helping to make zebrafish models of high-risk autism genes available to the research community.
SFARI is pleased to announce that it intends to fund 15 grants in response to the 2022 Genomics of ASD: Pathways to Genetic Therapies request for applications.
SFARI is pleased to announce that it intends to fund 36 grants (15 Pilot Awards and 21 Research Awards) in response to the 2018 Pilot and Research Awards request for applications.
The SFARI science team held an informational session to answer questions about the 2021 Genomics of ASD: Pathways to Genetic Therapies request for applications.
SFARI Investigator Liqun Luo discusses the neurodevelopmental disorder Smith-Magenis syndrome and his lab’s efforts to understand its underlying biology.
Lauren Weiss and Erik Ullian report on two studies using carrier-derived iPSC neurons to elucidate cellular phenotypes associated with 16p11.2 CNVs and a BRAF RASopathy mutation.
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