Zilong Qiu

This study shows that juvenile AAV-mediated MEF2C gene replacement can improve specific phenotypes in Mef2c-haploinsufficient mice.

This study shows that AAV-mediated TBR1 replacement in Tbr1-haploinsufficient mice improves some behavioral and electrophysiological outcomes but not all abnormalities.

This study identifies an ASXL3-thyroid hormone axis in parvalbumin interneurons that regulates autism-like behaviors and shows that early TH supplementation can reverse these effects in mice.

This study shows that Rtel1 in oxytocin neurons regulates oxytocin output and social behaviors in mice by resolving G-quadruplexes near the Oxt promoter.

This paper develops ProAPOBECs, engineered cytidine deaminases fused with PUF proteins, for effective RNA base editing in the brain, correcting mutations and reducing autistic-like behaviors in mice.

This study shows that AAV-mediated CSNK2B gene replacement in Csnk2b haploinsufficient mice rescues ASD-like phenotypes and restores EEG biomarkers, supporting its use as a translational readout for gene therapy.

RNAJog optimizes RNA sequences for multiple objectives using autoregressive reinforcement learning, achieving faster performance and improved vaccine design outcomes.

This study shows that Srcap haploinsufficiency in mice causes autistic-like behaviors by reducing Satb2 expression, which can be reversed with Satb2 gene therapy.

This study identifies inhibitory inputs from hippocampal CA1 to retrosplenial agranular cortex as critical for regulating social behavior, with implications for ASD treatment.

The paper maps excitatory axonal projections from the macaque ventrolateral prefrontal cortex to the whole brain at submicron resolution, revealing discrepancies with diffusion tractography.

This study shows that maternal separation in young rhesus monkeys can induce three core ASD symptoms, suggesting early environmental adversity contributes to ASD pathogenesis.

This paper demonstrates whole-brain in vivo base editing in mice to reverse autistic-like behaviors by correcting a mutation in the MEF2C gene.

This study identifies de novo variants in Chinese ASD trios, finding that ASD without DD/ID has fewer disruptive variants and novel risk genes not in existing databases.

This study edits PINK1 and DJ-1 genes in adult monkey brains using AAV-delivered CRISPR/Cas9, resulting in Parkinsonian symptoms and pathology.

This study identifies five major cell types in rhesus monkey amygdala using single-cell RNA sequencing, revealing unique molecular features compared to rodents.

This study identifies a SENP1 mutation in mice that causes core autistic-like symptoms by disrupting the SENP1-FMRP axis in the retrosplenial agranular cortex.

This study uses in vivo CRISPR/Cas9 to edit MECP2 in adolescent rhesus monkeys, resulting in autistic-like behaviors.

This study uses CRISPR to knockout RHO in rhesus macaques, resulting in RP-like phenotypes and demonstrating the feasibility of creating NHP models for retinal disease research.

The paper identifies shared circuit-level abnormalities between MECP2 transgenic monkeys and a subgroup of human autism patients, highlighting the need for a multimodal approach to study genetic effects in a primate model.

This study identifies CNTNAP3 mutations in ASD cohorts and shows its role in synaptic development and social behavior in mice.

This study shows that controlling emulsification in organic solvent-based tissue clearing improves transparency and preserves fluorescence without complete dehydration.

This study shows that CREST mutations in mice lead to neuroinflammatory responses and motor defects similar to ALS, revealing a molecular mechanism involving the CREST-BRG1 complex and cytokine expression.

This study shows that MECP2 duplication and mutations impair neural stem cell differentiation through miR-197 regulation of ADAM10 and NOTCH signaling.