S. E. Maloney

This study characterizes a Williams Syndrome mouse model, showing Gtf2ird1 overexpression rescues some sensorimotor tasks but not social behavior.

This paper develops a new social motivation assay in mice to study sex-differential roles of ASC-associated genes and oxytocin, finding distinct vulnerabilities in males and females.

This study investigates whether oxytocin receptor dysregulation contributes to fear memory deficits in a Williams Syndrome mouse model, finding no rescue of fear responses with an oxytocin receptor antagonist.

This study compares gait abnormalities in two mouse models of neurodevelopmental disorders across development and finds shared and disorder-specific gait features that change over time.

This study develops a standardized gait assay for mice and characterizes the developmental trajectory of gait in two strains, highlighting strain-specific features and parallels with human gait development.

This study shows that mutations in Gtf2i and Gtf2ird1 alone cannot reproduce the phenotypes of Williams syndrome caused by deletion of the WSCR region.

The paper identifies and addresses erroneous statistical practices in analyzing Social Approach Task data from autism mouse models, showing how incorrect methods increase false positives and proposing a solution.