RNA-sequencing data from lymphoblastoid cell lines derived from individuals with ASD and their unaffected siblings from the Simons Simplex Collection are now available to approved researchers.
Two SFARI Investigators were elected to the American Academy of Arts & Sciences, and one SFARI Investigator was elected to the National Academy of Sciences in April 2022.
This issue of the SFARI newsletter includes: (1) SFARI Autism Rat Models Consortium awardees announced, (2) 2022 Autism BrainNet Appreciation Award recipients announced, (3) INSYNC-AS inaugural meeting discusses the therapeutic landscape for Angelman syndrome, (4) Highlights of SFARI-funded research, (5) SFARI Supplement to Enhance Equity and Diversity — Request for applications, (6) SPARK Research Match Diversity, Equity and Inclusivity — Request for applications.
Ian Lipkin, Mady Hornig and colleagues showed that levels of immune molecules in mothers during pregnancy and in cord blood at birth are highly predictive of later autism diagnoses.
Laura Andreae, M. Albert Basson and collaborators showed that Chd8 haploinsufficiency in mice was linked to changes in excitation/inhibition balance and disrupted homeostatic plasticity of prefrontal circuits.
SFARI is pleased to announce that it intends to fund seven grants in response to the Autism Rat Models Consortium request for applications.
SFARI Investigator Susanne Schmid and colleagues showed that loss of Cntnap2 in rats leads to immature-like delays in auditory cortex sound processing and overactive auditory neurons.
Autism BrainNet announces the recipients of the 2022 Autism BrainNet Appreciation Award, an initiative that recognizes outstanding partners and collaborators for their dedication to advancing brain tissue research in autism.
A joint project of the Foundation for Angelman Syndrome Therapeutics (FAST) and SFARI, the International Angelman Syndrome Research Council (INSYNC-AS) held its inaugural meeting on July 9, 2021.
Ivan Iossifov, Michael Wigler and colleagues provided a detailed comparison of simplex and multiplex families with autism, supporting the view that de novo mutations are a more frequent cause of autism in low- than in high-risk families.