Prepartum bumetanide treatment reverses altered neonatal social communication but nonspecifically reduces postpubertal social behavior in a mouse model of fragile X syndrome DOI Creative Commons
Yui Sakamoto, Takeshi Takano, Shuji Shimoyama

и другие.

Genomic psychiatry :, Год журнала: 2024, Номер unknown, С. 1 - 12

Опубликована: Дек. 24, 2024

Fragile X syndrome is caused by monogenic silencing of the FMR1 gene and characterized high rates autism spectrum disorder. A previous study demonstrated that prepartum administration bumetanide, a chloride transporter blocker, normalized neonatal vocalization in non-congenic Fmr1 knockout (KO) pups. However, genuine contribution deletion to this phenotype congenic KO mouse model long-lasting effect bumetanide on postpubertal social interaction remains unclear. The current aimed determine impact at postnatal day 7 6 8 weeks age which genetic backgrounds were homogeneous between wild-type (WT) littermates. Moreover, we applied computational analytical algorithm determined predictive variables for interaction. Our data showed (1) mice exhibited altered numbers sequences distinct call types during reduced weeks, (2) select sets predicted levels, (3) restored pups but nonspecifically WT weeks. These indicate selectively impacts elements Additionally, restores has transient nonspecific negative subsequent

Язык: Английский

Mainstreaming Diagnostic Genetic Testing and Precision Medicine for Autism Spectrum Disorder DOI
David H. Ledbetter, Brenda Finucane,

Daniel Moreno‐De‐Luca

и другие.

Psychiatric Clinics of North America, Год журнала: 2025, Номер unknown

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0

Genomic and Developmental Models to Predict Cognitive and Adaptive Outcomes in Autistic Children DOI
Vincent-Raphaël Bourque,

Zoe Schmilovich,

Guillaume Huguet

и другие.

JAMA Pediatrics, Год журнала: 2025, Номер unknown

Опубликована: Апрель 21, 2025

Importance Although early signs of autism are often observed between 18 and 36 months age, there is considerable uncertainty regarding future development. Clinicians lack predictive tools to identify those who will later be diagnosed with co-occurring intellectual disability (ID). Objective To predict ID in children autism. Design, Setting, Participants This prognostic study involved the development validation models integrating genetic variants developmental milestones ID. Models were trained, cross-validated, tested for generalizability across 3 cohorts: Simons Foundation Powering Autism Research (SPARK), Simplex Collection, MSSNG. Autistic participants assessed older than 6 years age Study data analyzed from January 2023 July 2024. Exposures Ages at attaining milestones, occurrence language regression, polygenic scores cognitive ability autism, rare copy number variants, de novo loss-of-function missense impacting constrained genes. Main Outcomes Measures The out-of-sample performance was using area under receiver operating characteristic curve (AUROC), positive values (PPVs), negative (NPVs). Results A total 5633 autistic (4574 male [81.2%]) included this analysis. On average, 4 (IQR, 3-7) 11 (8-14) 1159 (20.6%) being model all predictors yielded an AUROC 0.653 (95% CI, 0.625-0.681), cross-validated generalized cohorts. modest reflected that only a subset individuals carried large-effect high scores, or presented delayed milestones. However, combinations typically not considered clinically relevant by diagnostic laboratories achieved PPVs 55% correctly identified 10% developing addition specifically improved NPVs rather PPVs. Notably, stratify probabilities up 2-fold higher compared typical Conclusions Relevance suggest growing neurodevelopmental condition–associated cannot, most cases, used alone predicting combining different classes provide individual-level predictions could useful targeting interventions.

Язык: Английский

Процитировано

0

New technology and emerging theories driving progress in neuropsychiatric disorders DOI Creative Commons
Zhanpeng Jin

Fundamental Research, Год журнала: 2024, Номер 4(6), С. 1349 - 1350

Опубликована: Ноя. 1, 2024

Язык: Английский

Процитировано

0

Prepartum bumetanide treatment reverses altered neonatal social communication but nonspecifically reduces postpubertal social behavior in a mouse model of fragile X syndrome DOI Creative Commons
Yui Sakamoto, Takeshi Takano, Shuji Shimoyama

и другие.

Genomic psychiatry :, Год журнала: 2024, Номер unknown, С. 1 - 12

Опубликована: Дек. 24, 2024

Fragile X syndrome is caused by monogenic silencing of the FMR1 gene and characterized high rates autism spectrum disorder. A previous study demonstrated that prepartum administration bumetanide, a chloride transporter blocker, normalized neonatal vocalization in non-congenic Fmr1 knockout (KO) pups. However, genuine contribution deletion to this phenotype congenic KO mouse model long-lasting effect bumetanide on postpubertal social interaction remains unclear. The current aimed determine impact at postnatal day 7 6 8 weeks age which genetic backgrounds were homogeneous between wild-type (WT) littermates. Moreover, we applied computational analytical algorithm determined predictive variables for interaction. Our data showed (1) mice exhibited altered numbers sequences distinct call types during reduced weeks, (2) select sets predicted levels, (3) restored pups but nonspecifically WT weeks. These indicate selectively impacts elements Additionally, restores has transient nonspecific negative subsequent

Язык: Английский

Процитировано

0