Valérie Nalesso

This study evaluates the efficacy of 5IA in the Dp(16)1Yey mouse model of Down syndrome, finding improved motor coordination but no cognitive rescue, suggesting divergent pathophysiology compared to Ts65Dn models.

This study shows that Dyrk1a regulates interneuron migration via actomyosin dynamics, leading to cortical GABAergic system defects and phenotypes seen in DYRK1A-haploinsufficiency syndrome.

Experiments across four laboratories found that arbaclofen rescued cognitive deficits in mouse models of 16p11.2 deletion, without sedation or significant off-target behavioral effects.

The paper introduces a new mouse model, Ts66Yah, for Down syndrome that replicates DS cognitive features and reveals genetic interactions between triplicated regions homologous to Hsa21 and unrelated regions.

The paper identifies six biological cascades involving key genes that alter behaviour and cognition in Down syndrome mouse models.